The review’s central insight is that the fate of an antioxidant is dictated less by the molecule itself than by the food matrix surrounding it. Consider vitamin C, or ascorbic acid, in an oil-in-water emulsion of the kind found in salad dressings and sauces. The water-soluble vitamin sits in the aqueous phase while lipid hydroperoxides accumulate at the surface of oil droplets. In the presence of iron, a common trace contaminant, ascorbic acid reduces ferric iron to the more reactive ferrous state, which then drives the Fenton reaction and generates hydroxyl radicals precisely at the oil-water interface. The result is accelerated lipid peroxidation: the celebrated antioxidant becomes an engine of spoilage. Whether ascorbic acid protects or damages a food depends on metal availability, oxygen concentration, and processing temperature.

Vitamin C’s oxidized form, dehydroascorbic acid, has a second life that is equally consequential. It and its breakdown products are reactive carbonyls that participate in Maillard-type reactions with amino acids, particularly lysine and cysteine, in protein-rich foods. These reactions occur rapidly at ordinary processing temperatures and lead to protein cross-linking, altering texture, solubility, and emulsifying properties. Nutritionally, the damage is real: when lysine residues are modified, this essential amino acid becomes biologically unavailable, lowering the protein quality of the food. Dehydroascorbic acid is also unstable, degrading into 2,3-diketogulonic acid and forfeiting vitamin activity altogether.

Vitamin E tells a parallel story in lipid-rich systems. Alpha-tocopherol, the principal lipid-soluble antioxidant, halts lipid peroxidation by donating a hydrogen atom to a lipid peroxyl radical, producing a relatively stable tocopheroxyl radical. That radical then faces a fork in the road. A co-antioxidant such as ascorbic acid can regenerate it back to active tocopherol; it can couple with another radical to form stable products such as alpha-tocopheryl quinone and dimers; or, if regeneration is slow, it can attack an unoxidized lipid molecule and start a fresh oxidation chain. Kinetic modeling of methyl linoleate peroxidation has shown quantitatively that under advanced oxidation or at elevated tocopherol concentrations, propagation reactions can outweigh chain-breaking activity, producing an apparent reversal from antioxidant to pro-oxidant behavior.

Deep-fat frying makes this reversal vivid. At high temperatures and in the presence of oxygen, high concentrations of alpha-tocopherol can actually accelerate lipid oxidation in frying oils, as rapidly formed tocopheroxyl radicals attack unoxidized fatty acids and hasten the development of off-flavors. Delta-tocopherol, by contrast, is more thermally stable and less prone to pro-oxidant behavior. In meat, where heme iron makes the environment aggressively pro-oxidant, feed supplementation with vitamin E improves oxidative stability, but during refrigerated storage alpha-tocopherol levels fall while alpha-tocopheryl quinone rises, a direct chemical signature of antioxidant work done, and a reminder that the product left behind is no longer an antioxidant at all.

Polyphenols add a third dimension, because their oxidation is often deliberately engineered. Black tea is the classic case: during fermentation, the enzyme polyphenol oxidase converts green tea catechins such as EGCG into reactive ortho-quinones, which condense into theaflavins, the orange-red pigments, and then into thearubigins, a poorly characterized family of brown polymeric pigments. These oxidized polymers give black tea its color, astringency, and distinctive biology. In wine and fruit, proanthocyanidins polymerize through acid-catalyzed carbocation chemistry, and the resulting chain length governs astringency, antioxidant capacity, and bioavailability. Controlled oxidation, in other words, can be a manufacturing tool rather than a defect.

Synthetic antioxidants follow the same logic. BHT, BHA, TBHQ, and the gallate esters all terminate lipid radical chains by hydrogen donation, then undergo oxidation, dimerization, and quinone or quinone methide formation. Under prolonged heating above roughly 160 to 180 degrees Celsius, BHT yields electrophilic quinone methides capable of reacting with cellular thiols and proteins, while gallate quinones form covalent Michael-addition products with amino acids and phospholipids. Some of these transformation products qualify as non-intentionally added substances that can migrate into food, a category regulators have barely begun to address.

Catching these fleeting species demands an arsenal of techniques, and the review devotes detailed attention to their complementary strengths. Liquid chromatography coupled to high-resolution mass spectrometry identifies stable oxidation products with mass accuracy below five parts per million, mapping tocopherol oxidation products in oil heated to 180 degrees Celsius and resolving seventeen microbial metabolites of theaflavins. Electron spin resonance spectroscopy, aided by spin traps, is the only method that directly observes transient radical intermediates such as the tocopheroxyl radical. Nuclear magnetic resonance provides definitive structures, as in the characterization of a glutathione adduct of a dehydroascorbic acid degradation product, while density functional theory calculations explain why alpha-tocopherol’s phenolic O-H bond is so weak and its radical so stable. No single platform suffices; the authors argue for hybrid workflows, standardized protocols, and better spectral libraries.

The biological consequences of all this chemistry are genuinely double-edged. On the beneficial side, mildly electrophilic derivatives act as hormetic stressors that activate the Keap1-Nrf2 pathway, the master switch for cellular antioxidant defenses, inducing enzymes such as heme oxygenase-1. Theaflavins from black tea protect cells through this route, and dehydroascorbic acid directly inhibits IKKbeta, damping the pro-inflammatory NF-kappa-B pathway, an anti-inflammatory function of vitamin C mediated entirely by its oxidized form. Meanwhile, gut bacteria metabolize the ninety to ninety-five percent of large polyphenols that escape small-intestinal absorption into bioavailable phenolic acids and urolithins, which are now thought to account for many of the systemic benefits of polyphenol-rich diets.

On the toxicological side, the picture darkens. Alpha-tocopheryl quinone is generally well tolerated, but the quinones of gamma- and delta-tocopherol are potent arylating agents that bind cysteine residues on proteins, provoking the unfolded protein response and apoptosis, a concern for foods fried in soybean oil, which is rich in gamma-tocopherol. Ascorbic acid-derived Maillard products contribute to the burden of advanced glycation end products, and vitamin C can even mediate the breakdown of lipid hydroperoxides into known genotoxins. The review’s most provocative conclusion may be regulatory: the FDA and EFSA evaluate the parent antioxidants added to food, yet almost no framework exists for assessing the safety of the oxidized interactome that consumers actually ingest. The authors call for metabolite-specific toxicology, realistic exposure assessment, and a shift away from the simplistic maxim that more antioxidants are better, toward mechanism-based design of foods in which oxidation is controlled, exploited, and understood.

Subject of Research: Oxidative transformation pathways and biological effects of oxidized antioxidant derivatives in food systems

Article Title: Unveiling the fate, function, and bioimpact of oxidized antioxidant derivatives in food systems

Article References: Sharma, S., & Kumar, V. (2026). Unveiling the fate, function, and bioimpact of oxidized antioxidant derivatives in food systems. Discover Chemistry, 3(1), Article 445. https://doi.org/10.1007/s44371-026-00903-2

Image Credits: AI Generated

DOI: 10.1007/s44371-026-00903-2

Keywords: antioxidants, oxidized derivatives, ascorbic acid, tocopherols, polyphenols, pro-oxidant activity, Nrf2 signaling, LC-HRMS, electron spin resonance, food chemistry, gut microbiome, food toxicology

Benzo[a]pyrene, often abbreviated BaP, is everywhere in modern life. It forms whenever organic matter burns incompletely, which means it rises from charcoal grills as fat drips onto hot coals, drifts from cigarette smoke and tailpipes, and accumulates in workplaces such as aluminum smelters, coke ovens and asphalt plants. The International Agency for Research on Cancer classifies it as a Group 1 carcinogen, a category reserved for agents with confirmed cancer-causing activity in humans. Once ingested or inhaled, BaP is metabolically activated by cytochrome P450 enzymes, chiefly CYP1A1 and CYP1B1, into a highly reactive intermediate called BPDE. This compound latches onto DNA to form adducts that can initiate cancer, while the metabolic process itself generates a flood of reactive oxygen species that overwhelm the body’s natural antioxidant enzymes and damage cell membranes, proteins and lipids. Because the liver serves as the body’s principal detoxification organ, it bears the brunt of this chemical assault.

The research team, based at Islamic Azad University in Shahrekord, Iran, set out to test whether dietary intervention could blunt this damage. Seventy male C57BL/6 mice were randomly assigned to fourteen groups of five animals each, with the sample size determined by formal power analysis to satisfy the principles of reduction in animal research. One group received only standard food, another received the olive oil vehicle used to dissolve the chemicals, and a third received 20 milligrams per kilogram of BaP daily by oral gavage for four weeks, a dose previously shown to induce significant oxidative stress and liver and kidney injury in mice without reaching acute lethal levels. A fourth group received vitamin E at 250 milligrams per kilogram, a dose established in earlier studies as antigenotoxic against BaP damage. The remaining groups received chia seed powder mixed into their food at 10, 20 or 30 percent by weight, either alone, alongside BaP simultaneously, or as a two-week pre-treatment before BaP exposure began.

The design allowed the researchers to answer two distinct practical questions. Co-administration tested whether the protective agents could limit damage occurring at the same time as exposure, a scenario relevant to people who cannot avoid contaminated food or polluted workplaces. Pre-treatment tested whether building up the body’s defenses in advance could prevent injury more effectively, a scenario relevant to preventive nutrition. All biochemical analyses were performed in a blinded manner, and the animals were monitored daily for humane endpoints such as excessive weight loss or lethargy, none of which were reached during the study.

The results were unambiguous in one direction and humbling in another. BaP exposure significantly depleted the mice’s total antioxidant capacity and superoxide dismutase activity, raised malondialdehyde, a marker of lipid peroxidation, elevated the liver enzymes AST and ALT, lowered serum albumin, and pushed triglycerides and LDL cholesterol upward. Vitamin E, despite its reputation as a potent fat-soluble radical scavenger, failed to restore antioxidant capacity or superoxide dismutase activity and offered no meaningful protection to the liver enzymes. Chia seeds, by contrast, produced dose-dependent benefits. At 20 and 30 percent dietary inclusion, co-administered chia significantly raised total antioxidant capacity and superoxide dismutase activity while lowering malondialdehyde. Thirty percent chia pre-treatment increased both superoxide dismutase and glutathione peroxidase activities and cut malondialdehyde levels further. Chia co-administration reduced AST at all doses, rescued albumin at the lower doses, lowered triglycerides across the board, and raised protective HDL cholesterol at the higher doses.

The lipid findings were particularly dramatic. BaP exposure drove triglycerides from roughly 1.1 millimolar in controls to 2.44 millimolar, and LDL cholesterol from about 83 to 163 milligrams per deciliter. Chia co-administration at 30 percent brought triglycerides back near baseline while pushing HDL cholesterol to levels well above those of untreated controls. The authors attribute these effects to the seed’s unique biochemical portfolio: alpha-linolenic acid, abundant dietary fiber and a rich array of polyphenols. Mechanistically, chia-derived alpha-linolenic acid appears to activate peroxisome proliferator-activated receptor alpha, boosting fatty acid oxidation, while suppressing sterol regulatory element-binding protein-1, which curbs lipogenesis. Chia components also inhibit fatty acid translocase, known as CD36, limiting fatty acid uptake into tissues, and the seed’s proteins and polyphenols reduce inflammatory signaling through tumor necrosis factor alpha while raising adiponectin.

Why did the whole food outperform the purified vitamin? The researchers argue that BaP’s toxicity is multifaceted, attacking membranes, enzymes, lipid metabolism and DNA simultaneously, and that a single antioxidant molecule simply cannot cover all those fronts. Chia seeds deploy a multitarget strategy: their polyphenols and omega-3 fats act synergistically to neutralize reactive oxygen species directly, and they appear to activate the nuclear factor erythroid 2-related factor 2, or Nrf2, signaling pathway, which switches on the cell’s own antioxidant gene program. Vitamin E, by contrast, may influence CYP1A1 and CYP1B1 activity, but the study suggests this mechanism is insufficient against the scale of oxidative assault that BaP delivers. The authors also note that the vitamin E dose, though previously validated, may have been inadequate for this model, or that the four-week treatment window was too short.

Not every organ responded. BaP raised blood urea nitrogen and creatinine, classic markers of kidney injury, but neither chia nor vitamin E significantly reversed these changes. The researchers suggest that renal protection may require longer treatment durations or different therapeutic approaches, pointing to similar findings with lavender extract against lead-induced nephrotoxicity. The study also has acknowledged limitations: the diets were not isocaloric, body weight and food intake were not formally tracked, tissue-level analyses were not performed, and the potentially synergistic combination of chia and vitamin E was never tested, a question the authors flag as a priority for future work.

The pre-treatment versus co-administration comparison carries a clear public health message. Pre-treatment with 30 percent chia preserved superoxide dismutase and glutathione peroxidase activities and kept malondialdehyde low, suggesting that building antioxidant reserves before exposure is the more effective strategy. For the millions of people exposed to BaP through charred food, secondhand smoke or occupational settings such as coke ovens and aluminum plants, where air monitoring has identified BaP as the dominant carcinogenic risk, the implication is that preventive dietary supplementation matters more than trying to repair damage after the fact. The findings also align with a broader shift in nutrition science away from single-molecule supplements and toward whole-food matrices, whose complex mixtures of bioactive compounds often deliver benefits that isolated nutrients cannot replicate.

Cautious interpretation remains essential. These results come from mice receiving deliberately high doses of both toxin and protective agents, and human trials of chia supplementation in healthy and overweight adults have generally shown only modest changes in lipid profiles and inflammatory markers, likely because those studies lacked a specific toxic challenge. The authors emphasize that clinical and mechanistic studies in humans are needed before dietary recommendations can be made with confidence. Still, the study offers a compelling proof of concept that a common, inexpensive whole food can outperform a flagship antioxidant supplement against one of the world’s most notorious environmental carcinogens, and it suggests that what you eat before exposure may matter as much as the exposure itself.

Subject of Research: Dietary protection against benzo[a]pyrene-induced oxidative toxicity in mice using chia seeds and vitamin E

Article Title: Protective Effects of Chia Seeds and Vitamin E Against Benzo[a]Pyrene‐Induced Toxicity in Male Mice: A Comparison of co‐Administration and Pre‐Treatment Strategies

Article References: Rezaei, M., & Karimi‐Dehkordi, M. (2026). Protective Effects of Chia Seeds and Vitamin E Against Benzo[a]Pyrene‐Induced Toxicity in Male Mice: A Comparison of co‐Administration and Pre‐Treatment Strategies. Food Science & Nutrition, 14(10), Article e72405. https://doi.org/10.1002/fsn3.72405

Image Credits: AI Generated

DOI: 10.1002/fsn3.72405

Keywords: benzo[a]pyrene, chia seeds, vitamin E, oxidative stress, hepatotoxicity, polycyclic aromatic hydrocarbons, antioxidants, mice study, lipid profile, food toxicology, pre-treatment, nutrition

Researchers at the University of Santiago de Compostela in Spain, led by Luis Rodríguez-Santos and Manuel Botana, carried out a 28-day repeated-dose oral toxicity study in mice, comparing the three principal diarrhetic shellfish toxins: okadaic acid, dinophysistoxin-1 and dinophysistoxin-2. The work, published in Current Research in Food Science, was designed to answer a question that regulatory agencies, including the World Health Organization and the Food and Agriculture Organization, have explicitly flagged as unresolved: what happens to the body when these toxins are ingested day after day at low doses, rather than in a single large serving?

The experimental design is notable for its attempt to mimic real human dietary exposure. Rather than forcing toxin solutions into the animals by gavage, the standard but stressful technique, the team delivered the toxins inside small pieces of bread that the mice voluntarily ate, a welfare-friendly approach that avoids confounding the results with handling stress. The daily dose of 90 micrograms per kilogram of body weight was calibrated to model a high-intake human dietary scenario derived from the European regulatory limit of 160 micrograms of okadaic acid equivalents per kilogram of shellfish meat. That calculation assumes a large 400-gram portion of contaminated bivalves for a 70-kilogram adult, then applies the standard 100-fold uncertainty factor used in toxicology to bridge the gap between animal and human exposure.

Over four weeks, the mice showed a pattern of persistent, cumulative toxicity that single-dose studies simply cannot capture. Dinophysistoxin-1 emerged as the most troublesome analogue, producing the greatest number of non-specific clinical signs and the most severe diarrhea, with significant effects in both sexes throughout the first three weeks of the study. Okadaic acid also caused significant clinical signs and diarrhea, particularly in females, whose fecal consistency scores became significantly worse than controls from the second week onward. Dinophysistoxin-2, by contrast, behaved remarkably differently: it produced almost no significant diarrhea at any point, reinforcing its reputation as the mildest of the three toxins.

That difference in clinical severity tracks closely with the toxins’ behavior inside the body. Using ultra-performance liquid chromatography coupled with tandem mass spectrometry, the researchers measured toxin concentrations in feces, intestinal contents and organs. Dinophysistoxin-2 was excreted rapidly and abundantly in feces while remaining barely detectable in tissues, suggesting poor gastrointestinal absorption and fast clearance that limits its systemic bioavailability. Dinophysistoxin-1 showed the opposite profile: the lowest fecal excretion but proportionally greater retention in the intestinal wall, indicating prolonged contact between the toxin and the gut lining. Okadaic acid fell somewhere in between, with high initial fecal excretion that declined over the study period. The highest tissue concentrations of all three toxins were found in the small and large intestines, precisely where the diarrheic damage occurs.

The microscopic evidence added another layer of concern. After 28 days of exposure, mice receiving okadaic acid and dinophysistoxin-1 showed significant thinning of the gastric mucosa, the protective lining of the stomach, a change the authors interpret as chronic epithelial alteration. Kidney sections revealed vascular congestion, tubular damage and an enlarged Bowman’s space, the cup-like structure where blood filtration begins, in animals treated with okadaic acid or dinophysistoxin-1, while dinophysistoxin-2-treated animals showed essentially preserved renal morphology. In the liver, dinophysistoxin-1 caused mild vascular changes, including dilated sinusoids and red blood cell extravasation, though hepatocyte architecture remained largely intact. Male mice given okadaic acid also showed a significant increase in relative heart weight, an intriguing systemic signal that warrants follow-up.

Perhaps the most striking findings involved sex. Female mice reduced their water intake significantly from day 14 onward, particularly those receiving okadaic acid, and showed trends toward lower urine output and higher urine protein-to-creatinine ratios, hints of subtle renal stress that the authors caution are qualitative rather than definitive proof of kidney dysfunction. Males, meanwhile, displayed more non-specific clinical symptoms overall, while females suffered more pronounced gastrointestinal effects. This sexual dimorphism in toxin response is a critical consideration for risk assessment, since most toxicological reference values are derived without fully accounting for sex-specific vulnerability.

The team also pioneered a novel biomarker approach, examining cyclophilin A and cyclophilin C, evolutionarily conserved proteins released into the extracellular space during inflammatory responses, in the intestinal contents of exposed mice. Detectable cyclophilin A and C appeared exclusively in the small intestinal contents of dinophysistoxin-1-treated animals, consistent with that toxin’s longer residence time in the gut and its harsher clinical profile. Cyclophilin C was absent from the intestinal contents of dinophysistoxin-2-treated animals across all replicates, mirroring that toxin’s milder effects. Because luminal contents lack stable housekeeping proteins for normalization, the authors present these results as descriptive qualitative support rather than quantified proof of inflammation, but the correlation with the toxicokinetic and clinical data is compelling.

The implications for the seafood consumer are nuanced. The authors are careful to note that their findings do not demonstrate that the current European regulatory limit is inadequate, nor do they establish a tolerable daily intake for these toxins. What the study does provide is the first comparative assessment of all three diarrhetic shellfish toxins under subchronic conditions using a voluntary feeding model that closely replicates natural dietary exposure. The data suggest that current toxicity equivalency factors, which assign okadaic acid and dinophysistoxin-1 a potency of 1 and dinophysistoxin-2 a potency of 0.6 based on older in vitro and acute intraperitoneal data, may need revision in light of oral toxicity evidence showing dinophysistoxin-1 to be substantially more harmful than its legal classification implies.

With climate change intensifying harmful algal blooms worldwide and extending the periods during which shellfish carry low but persistent toxin loads, the scenario modeled in this study becomes increasingly plausible for regular seafood consumers. The researchers acknowledge limitations, including the modest sample size of five animals per sex per group, the single exposure level tested, and the 28-day subchronic window, which falls short of the 90-day or lifetime studies needed to establish formal no-observed-adverse-effect levels. Still, by demonstrating that repeated low-dose exposure produces cumulative gastrointestinal, renal and hepatic effects with distinct toxin-specific and sex-specific profiles, the study delivers exactly the kind of harmonized comparative evidence that international expert panels have demanded, and it makes a strong case that the safety of the world’s favorite shellfish deserves evaluation through a longer, more chronic lens.

Subject of Research: Subchronic oral toxicity of diarrhetic shellfish toxins (okadaic acid, DTX1 and DTX2) in mice under repeated low-dose dietary exposure

Article Title: Regular exposure to low dose of diarrheic shellfish toxins: Implications for the seafood consumer

Article References: Rodríguez-Santos, L., Louzao, M. C., Cagide, E., Alvarez, M., Vale, C., Cifuentes, J. M., Vilariño, N., Graña, A., Carrera, C., Alvariño, R., Vieytes, M. R., Lolo, M., & Botana, L. M. (2026). Regular exposure to low dose of diarrheic shellfish toxins: Implications for the seafood consumer. Current Research in Food Science, 13, Article 101574. https://doi.org/10.1016/j.crfs.2026.101574

Image Credits: AI Generated

DOI: 10.1016/j.crfs.2026.101574

Keywords: diarrhetic shellfish toxins, okadaic acid, dinophysistoxin-1, dinophysistoxin-2, harmful algal blooms, shellfish safety, subchronic toxicity, food toxicology, marine biotoxins, toxicity equivalency factors, seafood consumption, cyclophilins

Discover Toxicology was inaugurated in May 2024 as a peer-reviewed, open access platform intended to publish research across all aspects of toxicology and its applications in research, development, and society. Its founding premise, the editors explain, is to give researchers, practitioners, policymakers, and stakeholders a venue to exchange knowledge, share best practices, and collaborate on solutions to pressing toxicological challenges. Like other journals in the Discover series, it welcomes all valid research, including null results, regardless of perceived impact, provided the work meets the standards of rigor and quality associated with Springer Nature. That policy is a deliberate counterweight to publication cultures that reward only headline-grabbing findings, a bias the editors argue has left critical dynamics of toxicological mechanisms in low-resourced countries understudied.

The breadth of the journal’s ambition is reflected in its Editorial Board, whose listed expertise spans toxins and venoms, clinical and preclinical pharmacology and toxicology, bioinformatics and cheminformatics, computational chemistry, ecotoxicity, regulatory toxicology, emerging contaminants, food safety, genetic toxicology, analytical chemistry, risk assessment, mechanisms of toxicity, omics, immunotoxicology, forensic pathology, and occupational exposure assessment. In the editorial, each Section Editor introduces the domain he or she represents, offering an unusually candid view of the technical questions the journal considers most pressing.

Professor Adekunle A. Bakare of the University of Ibadan, Nigeria, anchors the genotoxicology section. His laboratory studies the genotoxicity and mutagenicity of xenobiotics, the foreign chemicals that urbanization and industrialization have made almost impossible to avoid. Using in vitro and in vivo bioassays, his group examines the cytotoxic, genotoxic, and mutagenic effects of municipal solid waste leachates, industrial effluents, pesticides, analgesics, medicinal plant extracts, antiretroviral and antituberculosis drugs, metal and metal oxide nanoparticles, and electronic waste elutriates. The stakes, he argues, are generational: DNA damage from environmental xenobiotics is implicated not only in cancer and birth defects but also in heart disease, cellular aging, immune dysfunction, altered metabolism, neurodegenerative disease, and cataracts, and germline damage may affect future as well as current generations. He invites submissions on genotoxicity testing approaches, predictive toxicology, toxicogenomics, reproductive toxicology, epigenetics, gene expression analysis of DNA toxicity, artificial intelligence applied to DNA damage, and the links between genotoxicity and carcinogenesis.

Ajay Vikram Singh, a senior scientist at the German Federal Institute for Risk Assessment (BfR) in Berlin, represents the computational and nanotoxicology frontier. Working within an institute of more than 750 scientists that advises the German government on food and product safety, chemical risks, contaminants, animal protection, and consumer health, Singh combines advanced computational models, artificial intelligence, and nanoscale characterization to decipher how chemicals, nanomaterials, and biological systems interact. The goal is proactive safety assessment: predicting toxicity before products reach the market and enabling the design of inherently safer, so-called safer-by-design materials. He highlights the integration of multi-omics data with computational approaches, the nanobiophysics of mechanistic toxicology, and the regulatory challenges posed by complex novel materials, and he welcomes manuscripts using in silico methods, AI and machine learning-driven predictive toxicology, high-throughput screening data analysis, and mechanistic studies of engineered nanomaterials.

Edmond Sanganyado, associate professor at the University of Saskatchewan, works at the intersection of analytical chemistry and systems biology, developing tools that link exposure to toxicological effect through advanced omics technologies. He frames three questions that he believes will define the field: how to detect and quantify known and unknown toxicants and their metabolites quickly, cheaply, and reliably in real samples; how complex mixtures of pollutants affect organisms, ecosystems, and humans over a lifetime; and how to identify toxic substances in ways that stand up in court, keep pace with drug trends, and support public health. Big data, artificial intelligence, high-resolution mass spectrometry, and new approach methodologies, or NAMs, are driving all three disciplines, analytical, environmental, and forensic toxicology, toward mixture-based paradigms and toward reducing and replacing animal testing. But he cautions that publication norms emphasizing narrow novelty risk leaving the toxicology of low-resourced countries chronically understudied.

Neuropharmacologist João Paulo Capela of Portugal’s Fernando Pessoa University and the University of Porto brings the journal’s coverage to drugs of abuse and clinical toxicology. His research probes the brain actions of amphetamine-type stimulants and methylphenidate, both as illicit substances and as prescribed treatments for attention deficit hyperactivity disorder and other brain disorders. His central concern is translation: whether work is done in vitro or in animals, the purpose of mechanistic toxicology is to transfer findings to the human situation in order to prevent, mitigate, or treat adverse drug effects. He sees artificial intelligence-based tools as a promising means of elevating that mechanistic understanding, and he argues that new methodologies and models are essential for surveying how drugs and toxicants inflict damage at the cellular and molecular level.

Ecotoxicologist Maranda Esterhuizen, affiliated with the University of Helsinki and Häme University of Applied Sciences in Finland, specializes in pollution impact assessment and ecological restoration through nature-based solutions, with a deliberately transdisciplinary approach bridging environmental science and policy. She describes environmental toxicology as standing at a critical juncture, confronting complex chemical mixtures and climate-induced shifts in pollutant behavior, particularly in rapidly urbanizing regions. Her section invites research using adverse outcome pathways, omics technologies, and predictive modeling to understand toxicity across biological scales, and she singles out studies integrating climate change dynamics, urbanization, and chemical mixture interactions as especially welcome, because they mirror the compounded pressures ecosystems actually face.

Food and computational toxicologist Yu-Syuan Luo of National Taiwan University completes the editorial leadership roster. His focus is on human-relevant, mechanism-informed chemical safety evaluation at a time when data gaps for emerging contaminants, low-dose exposures, and complex mixtures impede timely regulatory decisions. Food toxicology, he notes, is pivotal for assessing ingredients, contaminants, and food-contact materials, especially for endpoints such as endocrine disruption and mixture toxicity. Computational toxicology complements it with scalable predictive tools, including in silico modeling, omics-based profiling, and data-driven hazard identification and prioritization, supporting the global shift away from traditional animal testing and toward more efficient, transparent, forward-looking risk assessment.

Taken together, the editorial sketches a discipline in methodological upheaval: from single-compound testing toward mixtures, from animal models toward new approach methodologies, from reactive hazard characterization toward AI-assisted prediction and safer-by-design chemistry. By welcoming null results and prioritizing rigor over novelty, Discover Toxicology is positioning itself as a home for precisely the unglamorous, reproducible, and globally inclusive work that this transition requires, and the editors close with an open invitation to researchers worldwide to submit work spanning fundamental questions and real-world applications alike.

Subject of Research: An editorial by the section editors of the open access journal Discover Toxicology outlining research priorities across genotoxicology, computational and nanotoxicology, ecotoxicology, neurotoxicology, and food toxicology.

Article Title: Discover Toxicology, the future journal for your toxicology research

Article References: Bakare, A. A., Singh, A. V., Sanganyado, E., Capela, J. P., Esterhuizen, M., Luo, Y.-S., & Guo, Y. (2026). Discover Toxicology, the future journal for your toxicology research. Discover Toxicology, 3(1), Article 12. https://doi.org/10.1007/s44339-026-00053-1

Image Credits: AI Generated

DOI: 10.1007/s44339-026-00053-1

Keywords: Discover Toxicology, toxicology, open access publishing, genotoxicity, xenobiotics, computational toxicology, nanotoxicology, ecotoxicology, new approach methodologies, food toxicology, chemical mixtures, risk assessment