Background Lambda-cyhalotherin (LCT) is a pyrithroid type 2 pesticide that is broadly utilized in pest control in public health, animal health, and agriculture. Although claiming that LCT has a low mammalian toxicity, several investigations reported its mammalian hepatotoxicity by mediating oxidative stress causes severe hepatotoxicity and liver damage. Results LCT significantly decreased catalase (CAT), superoxide dismutase (SOD), and total thiol (T. thiol) and increased lipid peroxidation (LPO). mRNA and protein expression levels of p53 were upregulated, whereas Bcl-2 mRNA and protein expression levels were downregulated in LCT-intoxicated animals. Also, light microscopic and ultrastructure studies for liver tissues of LCT-intoxicated animals showed mononuclear leukocytic infiltration in the parenchyma, congested portal vein with thickened wall, and proliferation of bile duct and hepatocytes with cytoplasmic vacuolations, fatty changes, and collagen fibers. Panax ginseng co-treatment attenuated oxidative stress biomarkers. Both tested doses of Panax ginseng (100 and 200 mg /kg b. wt./day) significantly decreased p53 and elevate Bcl-2 mRNA and protein expression levels and reveals significant amelioration and restoration of normal histology and ultrastructure of liver, but 200 mg/kg b. wt. of Panax ginseng seems to be more potent. Conclusion Panax ginseng exhibited ameliorative effect against hepatic oxidative stress, apoptosis, histopathological, and ultrastructural changes induced by LCT.

Introduction: Lambada-cyhalotherin (LCT) caused severe oxidative damage in liver, lung and testis. Aim of the Study: The objective of this research was to evaluate the ameliorative activity and underlying techniques of pure Panax ginseng (G) using rat model of LCT-induced lung damage. Materials and Methods: 36 male adult laboratory rats Rattus norvegicus domestica in weights around 135±10 g were separated into 6 experimental groups: 1 st control group. 2 nd and 3 th groups were G groups (100 and 200 mg G/kg b. wt.) LCT group was given by oral gavage LCT (61.2 mg /kg b. wt.) that is equivalent to 1/10 of LD50. The 5 th and 6 th groups were cotreated with two doses of G. Results: LCT significantly decreased superoxide dismutase (SOD), catalase (CAT) and total thiol (T. thiol) and increased lipid peroxidation (LPO). mRNA and protein expression levels of p53 gene (apoptotic gene) were increased, whereas, Bcl-2 gene (anti-apoptotic gene) mRNA and protein expression levels were decreased in LCT-treated animals. Also, light microscopic and ultrastructure studies for lung tissues of LCT-treated animals showed marked hyperplasia of dilated bronchioles wall, RBCs extravasation in bronchiolium lumen and mononuclear leukocytic infiltration in parenchyma. Additionally, blood vessels congested with thickened walls, alveoli appeared collapsed with compensatory expansion of adjacent alveoli divided by thickened inter-alveolar septa, besides to damage in type 1 and type 2 pneumocytes. G co-treatment attenuated oxidative stress biomarkers. Both tested doses of G significantly decreased p53 and elevate Bcl-2 mRNA and protein expression levels and revealed significant amelioration and restoration of normal histology and ultrastructure of lung. Conclusion:In summary, G has exhibited ameliorative activity against oxidative stress induced by LCT in lung, apoptosis, histopathological and ultrastructural changes in albino rats.