Recently, melatonin has attracted attention because of their strong free radical scavenging and antioxidant properties. The present study was designed to investigate the role of melatonin against cypermethrin induced hepatotoxicity in rats using qualitative, quantitative and biochemical approaches. Adult female Wistar rats were randomly divided into four groups; each group consists of six animals. Control group received vehicle, corn oil; Cypermethrin (CM) [250mg/kg bw]; Melatonin (MEL) [10 mg/kg bw]; CM+MEL treated group. Animals were treated orally, daily for a period of 4 weeks. Animals were sacrificed by decapitation and liver was used for various biochemical and histopathological examinations. The result of this study shows that in vivo administration of cypermethrin caused a significant induction of oxidative damage in liver tissue as evidenced by depletion of proteins, glutathione (GSH) and increased lipid peroxidation in hepatic tissue. Cypermethrin administration significantly enhanced the activities of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) glutathione reductase (GR) and glutathione-Stransferase (GST). Cypermethrin intoxication exhibited elevation in the activities of liver marker enzymes such as serum glutamate pyruvate transaminase (SGPT) serum glutamate oxaloacetate transaminase (SGOT) and Lactate dehydrogenase (LDH). Furthermore, the co-administration of melatonin mitigates the hepatotoxicity of cypermethrin by normalizing the biochemical and enzymatic parameters. The biochemical observations were supported by histopathological examination of liver. The findings of this investigation suggest that the melatonin may play a protective role against cypermethrin induced hepatotoxicity and oxidative damage in female albino rats.

Interleukin-3 (IL-3) is produced during infections caused by parasites, bacteria and viruses, but its contribution to immunity in this context remains largely unknown. In mouse models of parasitic infections, in which the effects of IL-3 have been most extensively studied, IL-3 has been variously reported as protective, detrimental or inconsequential. Similarly, mixed results have been reported in viral and bacterial infection models. Here, we investigated the effects of IL-3 in mouse models of Mycobacterium tuberculosis and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections by assessing the pathogen burden, disease manifestations and survival following infection. After infection with M. tuberculosis, IL-3 deficient mice showed higher bacillary burden, increased lung pathology and reduced survival compared to wild type mice. After infection with HSV-1 through cutaneous route and HSV-2 through vaginal route, IL-3 deficient mice showed higher viral burden, increased disease manifestations and reduced survival compared to wild type mice. Our results show that IL-3 makes a subtle but significant contribution to protective immunity in these mouse models of bacterial and viral infections.