Bee Venom - Lead Acetate Toxicity Interaction

Venom immunotherapy is a highly effective treatment, capable of improving health-related quality of life. Bee venom (BV) is considered an effective rheumatoid arthritis modulator that removes reactive oxygen species (ROS). The hypothesis behind the present work was that, the ability of BV to remove reactive oxygen species (ROS) may help in protecting against lead acetate induced hepatic injury. Accordingly, the present study was designed to investigate the possible interaction between BV and lead acetate, with an emphasis on the involvement of IL-6 and oxidative stress in the BV- lead acetate hepatic effects in mice. Adult male mice were divided into 2 main groups namely, BV group and BV/Lead acetate group. The BV group was equally divided into 5 subgroups, given BV in the dose levels 0, 1, 2.5, 5 or 10 ^g/kg, sc. The BV/Lead acetate treated animals were parallely divided into 5 subgroups, according to the given dose of BV. They were orally administered 100 mg/kg lead acetate, 1 hr after BV administration. Each of BV and lead acetate was given every other day for one month. Twenty-four hours after the last dosage, serum biochemical markers (ALT and AST), liver oxidative stress markers (superoxide dismutase, SOD, glutathione GSH, malondialdhyde MDA, and catalase, CAT), liver total nitrate/ nitrite content, and interleukin-6 (IL-6) were assessed. The obtained results revealed that, while administration of BV induced decrease in liver IL-6 content, it induced increase in the hepatic total nitrite/nitrate content. The liver GSH levels and SOD activity were inversely correlated with the lower used doses of BV (1, 2.5 and 5 ^g/kg). The high-utilized dose 10 ^g/kg induced a significant increase in liver MDA content. Lead acetate decreased the survival rate and the relative liver weight and increased ALT activity. Pre-administration of BV restored each of the liver weight, ALT activity and the liver nitrite content to their normal ranges. In conclusion, exposure to lead acetate resulted in mild to moderate liver toxicity, whose certain manifestations were alleviated on co-exposure to Low dose level of BV