Wolfberry Compound Shields Duck Kidneys From Cadmium Damage, Study Finds

Cadmium is one of the most stubborn pollutants in the modern environment. Released by electroplating plants, battery manufacturing, and pigment production, the heavy metal accumulates in water, soil, and air, and it does not break down. For waterfowl such as ducks, which live in ponds, lakes, and rivers and sit relatively high in aquatic food chains, exposure is difficult to avoid. Now a research team at Yangzhou University in China has shown that a natural compound extracted from goji berries, the small red fruits of Lycium barbarum, can substantially protect duck kidneys from cadmium-induced damage. The study, published in Frontiers in Veterinary Science, combines classical toxicology with molecular analysis to map exactly how the polysaccharide counters the metal’s assault on renal tissue.

The investigators worked with forty healthy seven-day-old male Shaoxing ducks, a commercially important breed, dividing them into four groups of ten. One group served as untreated controls, one received only Lycium barbarum polysaccharides, or LBPs, at 50 milligrams per kilogram delivered intragastrically, one received cadmium chloride mixed into feed at 50 milligrams per kilogram, and the final group received both. The experiment ran for thirty days under controlled conditions of temperature, humidity, and light. Doses were selected on the basis of previous studies and the team’s own preliminary experiments, and the protocol was approved by the Institutional Animal Care and Use Committee of Yangzhou University.

The consequences of cadmium exposure were quickly apparent. Ducks in the cadmium group lost significant body weight while their kidneys grew heavier relative to body size, a sign of swelling and stress in the organ. Blood chemistry told the same story: levels of creatinine and uric acid, the standard clinical indicators of kidney function, rose sharply. Under the microscope, the damage was striking. Hematoxylin and eosin staining revealed severely disrupted renal architecture, blurred tissue boundaries, atrophied and deformed glomeruli, the kidney’s core filtration units, and hemorrhage in the interstitial spaces. Transmission electron microscopy pushed the view down to the cellular level, exposing nuclear deformation, severe mitochondrial vacuolation, and rupture of the mitochondrial cristae, the folded membranes where cellular energy is produced.

Beneath these visible injuries lay a subtler biochemical sabotage. Using flame atomic absorption spectrometry on digested kidney tissue, the researchers measured the organ’s elemental makeup. Cadmium accumulated dramatically, and as it did, the levels of four essential trace elements, iron, manganese, zinc, and copper, fell. The reason is chemical mimicry. Cadmium shares ionic radius and coordination tendencies with these essential metals, so it can impersonate them in biological systems without performing their functions. The consequences cascade: zinc and copper are components of superoxide dismutase, manganese is the cofactor for the mitochondrial form of that enzyme, and excessive free iron catalyzes the Fenton reaction, generating highly destructive hydroxyl radicals from hydrogen peroxide. Deprived of their raw materials, the antioxidant enzymes falter precisely as the toxic metal floods the system.

The oxidative stress measurements confirmed this collapse. Malondialdehyde, a marker of lipid peroxidation, and hydrogen peroxide rose markedly, while the activities of superoxide dismutase, catalase, and total antioxidant capacity fell, along with the content of glutathione, the cell’s master antioxidant. The team then traced the failure to a master molecular switch. Nrf2 is a transcription factor that, under stress, detaches from its cytoplasmic anchor Keap1, moves into the nucleus, and switches on antioxidant response element-dependent genes. In cadmium-exposed ducks, the protein levels of Nrf2 and its downstream targets, HO-1, NQO1, GCLC, GCLM, and GSR, all dropped. Because GCLC, GCLM, and GSR govern the synthesis and regeneration of glutathione, their suppression crippled the cell’s capacity to manufacture and recycle its most important antioxidant defense.

This is where the wolfberry compound intervened. When ducks received both cadmium and LBP, the pattern reversed. Cadmium burden in the kidney fell, iron, manganese, zinc, and copper levels recovered, the antioxidant enzymes rebounded, and the Nrf2 pathway proteins climbed back toward normal. The researchers attribute the effect to the intrinsic antioxidant, anti-inflammatory, and lipid-lowering properties of LBPs, the major bioactive components of the goji berry, which have been valued in traditional Chinese medicine and are increasingly supported by modern pharmacology. Previous work has shown these polysaccharides acting through multiple signaling pathways with anti-aging, hypoglycemic, immunomodulatory, and neuroprotective effects, and dietary LBP supplementation has already been shown to enhance antioxidant defenses and growth performance in broiler chickens.

But the study’s most novel contribution extends beyond the classic antioxidant story. Cadmium, the team found, triggered a profound disruption of lipid metabolism in the kidney. Total cholesterol and triglyceride levels rose in both serum and kidney tissue, and lipid droplets accumulated visibly under the electron microscope. At the protein level, cadmium upregulated the lipogenic machinery, including FAS, SREBP1, ACC1, ACC2, and PPARγ, the transcription factor that drives adipocyte differentiation and lipid storage. Simultaneously it downregulated the fat-burning side of the ledger: ATGL and HSL, the rate-limiting enzymes that break triglycerides down step by step, along with PPARα, the master regulator of fatty acid oxidation, and CPT2 and LPL, which shuttle fatty acids into mitochondrial beta-oxidation and clear circulating triglyceride-rich lipoproteins respectively. LBP co-treatment corrected both directions of this imbalance, restoring fat breakdown while suppressing excess fat synthesis.

That metabolic rescue rippled into the immune system. The kidney is not merely a filter but an active immune organ, populated by macrophages and T cells that maintain its internal environment. Macrophages polarize into pro-inflammatory M1 cells, marked by iNOS and CD68, or anti-inflammatory M2 cells, marked by Arg1, while T helper cells divide similarly into Th1 and Th2 lineages, tracked by T-bet and GATA3. Cadmium exposure pushed the balance hard toward inflammation: iNOS, CD68, T-bet, and CD4 rose while Arg1 and GATA3 fell, and the inflammatory cytokines IL-18, IL-1β, and TNF-α climbed in kidney tissue. LBP supplementation reversed the polarization markers and substantially lowered all three cytokines. The finding fits into a wider picture in which oxidative stress and disordered lipid metabolism feed chronic inflammation, exhaust immune cells, and ultimately produce immunosuppression, a vicious cycle that the polysaccharide appears to interrupt at multiple points.

The authors are candid about their limits. All results come from phenotypic observations and targeted protein measurements in a live duck model, and without Nrf2 inhibitor or gene-interference experiments the Nrf2 findings indicate correlation rather than proven causality. No transcriptomic or metabolomic analyses were performed, so the global molecular landscape remains unmapped. Even so, the study offers molecular evidence for a natural, widely available feed additive that could protect livestock from heavy metal nephrotoxicity, with implications that reach the human dinner plate, since duck meat and offal enter the food supply chain. As cadmium pollution intensifies with industrialization, a humble berry extract that quiets oxidative stress, restores trace element balance, mends lipid metabolism, and calms inflamed immune tissue is a finding worth watching closely.

Subject of Research: Protective effects of Lycium barbarum polysaccharides against cadmium-induced kidney injury in ducks via the Nrf2 antioxidant pathway

Article Title: Lycium barbarum polysaccharides alleviate cadmium-induced renal injury in ducks by activating the Nrf2-mediated antioxidant defense pathway

Article References: Wang, X., Liu, D., Ma, Y., Zou, H., Tong, X., Zhu, J., Song, R., Zhao, H., & Liu, Z. (2026). Lycium barbarum polysaccharides alleviate cadmium-induced renal injury in ducks by activating the Nrf2-mediated antioxidant defense pathway. Frontiers in Veterinary Science, 13, Article 1998071. https://doi.org/10.3389/fvets.2026.1998071

Image Credits: AI Generated

DOI: 10.3389/fvets.2026.1998071

Keywords: cadmium, nephrotoxicity, Lycium barbarum polysaccharides, Nrf2, oxidative stress, ducks, lipid metabolism, kidney injury, trace elements, antioxidant defense, immune balance, wolfberry