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Zinc Oxide Nanoparticles Ameliorate Dimethylnitrosamine-Induced Renal Toxicity in Rat
Varsha Rani1, Yeshvandra Verma1, S V S Rana2
1Department of Toxicology, Chaudhary Charan Singh University, Meerut, 250004, India.
Abstract:
Dimethylnitrosamine (DMN) is an established carcinogen. It is toxic to several organs, viz., the liver, kidney, and lungs, and immune system. Several drugs have been used in the past to modulate its toxicity using experimental animal models. The present study was designed to investigate the effect of zinc oxide nanoparticles (ZnONPs) on renal toxicity caused by DMN in laboratory rat. Since oxidative mechanisms are mainly involved in its toxicity, the proposed study focuses on the amelioration of oxidative stress response by ZnONPs, if any. The present results show that administration of ZnONPs (50 mg/kg body weight/rat) to DMN (2 μl/100 g body weight/rat)-treated rats diminuted the concentration of malonaldehyde, H2O2, and NO in the kidney. However, reduced glutathione (GSH) concentration increased after ZnONP treatment. Results on glutathione S-transferase and glutathione peroxidase favored its antioxidative effects. These results are supported by the recovery of oxidative DNA damage and less pronounced histopathological changes in the kidney. It is hypothesized that ZnONPs might be toxic to renal tissue; however, its strong therapeutic/antioxidative potential helps in ameliorating DMN-induced renal toxicity in rat.
Insights
Zinc oxide nanoparticles (ZnONPs) show potential in mitigating kidney damage caused by dimethylnitrosamine (DMN). ZnONPs reduced oxidative stress markers and improved kidney function in DMN-treated rats.
Area of Science:
- Toxicology
- Nanomedicine
- Biochemistry
Background:
- Dimethylnitrosamine (DMN) is a known carcinogen causing toxicity in organs like the liver, kidney, and lungs.
- Oxidative stress mechanisms are primarily implicated in DMN-induced organ damage.
- Previous studies have explored various therapeutic agents to counteract DMN toxicity in animal models.
Purpose of the Study:
- To investigate the protective effects of zinc oxide nanoparticles (ZnONPs) against DMN-induced renal toxicity in rats.
- To evaluate the potential of ZnONPs in ameliorating oxidative stress in the kidney following DMN exposure.
- To assess the impact of ZnONPs on biochemical and histopathological markers of kidney damage.
Main Methods:
- Laboratory rats were administered DMN to induce renal toxicity.
- ZnONPs were administered to DMN-treated rats at a dose of 50 mg/kg body weight.
- Kidney tissue was analyzed for malondialdehyde (MDA), hydrogen peroxide (H2O2), nitric oxide (NO), reduced glutathione (GSH), glutathione S-transferase (GST), and glutathione peroxidase (GPx) levels.
- Oxidative DNA damage and histopathological changes in the kidney were assessed.
Main Results:
- ZnONP administration significantly reduced MDA, H2O2, and NO concentrations in the kidneys of DMN-treated rats.
- Reduced glutathione (GSH) levels increased following ZnONP treatment.
- Enzyme activities of GST and GPx indicated antioxidative effects of ZnONPs.
- ZnONPs treatment led to recovery from oxidative DNA damage and reduced histopathological alterations in the kidney.
Conclusions:
- ZnONPs demonstrate significant antioxidative and therapeutic potential in ameliorating DMN-induced renal toxicity.
- Despite potential inherent toxicity, ZnONPs effectively counteract DMN-induced kidney damage through antioxidant mechanisms.
- These findings suggest ZnONPs as a promising therapeutic agent for managing DMN-induced nephrotoxicity.
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