Lambda cyhalothrin toxicity induces alterations in lipogenic genes and inflammatory factors in rat liver.

Abstract

The present study aims to elucidate the molecular basis of lambda cyhalothrin (LCT) toxicity. Thirty-two mature male albino rats were randomly classified into four equal groups. The first group was orally administered normal saline, the second group was orally administered dimethylsulfoxide (DMSO). The third group was orally administered 1/100 LD50 (6.12 mg/kg b. wt) of a commercial formulation containing 2.5% LCT (i.e., a net dose LCT corresponding to 0.15 mg/kg b. wt). The fourth group was orally administered 1/100 LD50 (0.64 mg/kg b. wt) of a pure form of LCT. The results indicated that exposure to LCT is capable of inducing an up-regulation in the mRNA expression levels of peroxisome proliferative activated receptor α and γ (PPAR α and PPAR γ), tumor necrosis factor (TNF-α), fatty acid synthase (FAS) and sterol regulatory element binding protein-1c (SREBP-1c). Additionally, our study revealed a significant increase in serum levels of ALT, AST, ALP, γGT as well as the inflammatory cytokines TNF-α and monocyte chemoattractant protein-1 (MCP-1). A significant elevation in total lipids, total cholesterol, triacylglycerol, LDL-c and leptin with a corresponding significant decrease in HDL-c was also noted. Moreover, our results depicted that LCT treatment exhibits a significant increase in hepatic MDA levels concurrent with a significant decrease in GSH levels and the activities of CAT, SOD, and GPx. An immunohistochemical investigation also revealed a strong up-regulation of hepatic FAS in the LCT treated groups. The histopathological findings were marked by evidence in support of periportal fatty changes and interstitial aggregation of round cells.