Carvacrol protects against λ‐Cyhalothrin‐induced hepatotoxicity and nephrotoxicity by modulating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy

Abstract

Abstractλ‐Cyhalothrin, a type II synthetic pyrethroid, has been widely used in households, agriculture, public health, and gardening to control insect pests. Despite its widespread usage, it is known to induce a variety of adverse effects, including hepatotoxicity and nephrotoxicity. The goal of this study was to investigate the protective effect of carvacrol, which has antioxidant, anti‐inflammatory, anti‐apoptotic, and some other properties, on λ‐Cyhalothrin‐induced hepatotoxicity and nephrotoxicity 35 male Sprague–Dawley rats were randomly divided into five groups for this purpose: I‐Control group: II‐CRV group (50 mg/kg carvacrol), III‐LCT group (6.23 mg/kg LCT), IV‐LCT + CRV 25 group (6.23 mg/kg LCT + 25 mg/kg carvacrol), and V‐LCT + CRV 50 group (6.23 mg/kg LCT + 50 mg/kg carvacrol). Using biochemical, real‐time PCR, and western blotting methods, the collected tissues were analyzed. While λ‐Cyhalothrin treatment increased MDA levels, which are indicated of lipid peroxidation, but reduced SOD, CAT, GPx activities, and GSH levels. After receiving carvacrol therapy, the degree of oxidative stress reduced as the values of these parameters approached those of the control group. Increased inflammation, apoptosis, endoplasmic reticulum stress, and autophagy with λ‐Cyhalothrin administration reduced with carvacrol co‐administration, and liver and kidney tissues were protected from damage, depending on the degree of oxidative stress. After considering all of these data, it was discovered that λ‐Cyhalothrin‐induced oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy in the liver and kidneys; however, carvacrol protected the tissues from damage. Our findings indicate that carvacrol may be a promising protective agent in λ‐Cyhalothrin‐induced hepatotoxicity and nephrotoxicity.