Thiamethoxam (TMX) is a non-mutagenic neonicotinoid insecticide that is widely used to combat different types of insects. The hepatotoxicity and carcinogenicity of TMX have been approved previously in mice but not in rats. However, the TMX-induced hepatotoxic and pro-carcinogenic effects on rabbits remain unclear. The present study elucidated the roles of oxidative stress, pro-inflammatory cytokines, and apoptosis-related genes in the hepatotoxic and carcinogenic effects of TMX on rabbits. Sixteen male rabbits were equally divided into two groups; eight rabbits orally treated with TMX at a dose of 250 mg/kg b.w for 90 successive days. Hepatotoxic effects of TMX were evidenced by attenuation of liver enzyme activities, elevation of bilirubin levels, and alterations in the hepatic architecture, including hepatocyte death by necrosis and apoptosis, lymphocyte infiltration and fibrosis. TMX induced oxidative stress, as evidenced by the significant increases in malondialdehyde levels and antioxidant enzyme (glutathione transferase and catalase) activities along with a decrease in glutathione levels. TMX also up-regulated the mRNA levels of interleukin-6 (1.6-fold) and B cell lymphoma-2 (1.8-fold) and down-regulated the mRNA level of the tumor necrosis factor-α (0.8-fold), indicating its effects on cell survival and proliferation through the inhibition of apoptosis. Interestingly, the elevated level of carcinoembryonic antigen and the appearance of ground glass-like hepatocytes suggested that TMX exerted a pro-carcinogenic effect. In conclusion, TMX exerts potentially hepatotoxic and pro-carcinogenic effects on rabbits by modulating oxidative/antioxidative status and pro-inflammatory cytokine production, inhibiting apoptosis and activating cell survival pathways.

No abstract

No abstract

The current investigation assessed the impacts of sub-lethal concentrations of silicon dioxide nanoparticles (SiO2NPs) on hepato-renal functions, histopathological characteristics, and gene transcription in gills and liver of Nile tilapia juveniles. Fish were exposed to 20, 40, and 100 mg/L of SiO2NPs for 3 weeks. Pairwise comparisons with the control group showed a significant dose-dependent elevation in serum ALP, ALT, and AST enzyme activities as well as blood urea and creatinine levels in SiO2NP-intoxicated groups. Exposure to 100 mg/L SiO2NPs significantly upregulated expression of HSP70, TNF-α, IL-1β, and IL-8 genes in the gills as compared to the control group. Moreover, exposure to 100 mg/L SiO2NPs significantly upregulated the expression SOD, HSP70, IL-1β, IL-8, and TNF-α genes in the hepatic tissues as compared to the control group. Exposure of fish to 20 mg SiO2NPs/L significantly increased the mRNA expression levels of IL-12 in both the gills and liver tissues. Notably, all tested SiO2NP concentrations significantly upregulated the transcription of CASP3 gene in gills and liver of Nile tilapia as compared to the control group. Interestingly, varying histopathological alterations in renal, hepatopancreatic, and branchial tissues were observed to be correlated to the tested SiO2NP concentrations. In conclusion, our results provide additional information on the toxic impacts of SiO2NPs in Nile tilapia at the hematological, tissue, and molecular levels.

No abstract