Abstract
Lithium therapy mainly used in curing some psychiatric diseases responsible for numerous undesirable side effects on different organs in humans. The present study explores the beneficial effect of sobatum, a purified compound of Solanum trilobatum, on lithium carbonate (Li2CO3)-induced multiple organ toxicity in rats. Li2CO3 (150 mg/kg body weight) was administered orally in drinking water for a period of 30 days to induce toxicity in rats. Li2CO3 could induce lipid peroxidation to a significant extent that was accompanied by marked reduction in reduced glutathione, SOD, CAT, GST, GPX activities, and parallel decline in ATP in tissues. Toxicity resulted in abnormal elevation of lipids such as cholesterol, triglycerides, phospholipids, and fatty acids in liver tissues. Treatment with sobatum affords substantial protection in liver and heart by altering all the parameters to near normal levels that were further confirmed by histological examination. Sobatum prevents Li2CO3-induced oxidative damage of DNA by reducing DNA fragmentation indicating its block on cell death. However, these results demonstrated that sobatum has the ability to suppress the drug-induced toxicity.
Highlights
Lithium is widely used in the treatment of bipolar disorders, refractory depressive disorders, and in the long-term prophylaxis of cluster headache
Considering above information, the present study aims to investigate the effect of sobatum on toxicity caused by Li2CO3 in liver, heart, and kidney tissues of experimental rats through evaluating lipid peroxidative content, hepatic lipid levels, antioxidant enzymes, adenosine triphosphate (ATP) levels, apoptotic cell death, and histological changes
Lithium-toxicated rats were accompanied by increased thiobarbituric acid reactive substances (TBARS) production and decreased antioxidant defense enzyme activities, suggesting oxidative stress in liver tissue [Table 1]
Summary
Lithium is widely used in the treatment of bipolar disorders, refractory depressive disorders, and in the long-term prophylaxis of cluster headache. There is gradual accumulation of lithium, usually due to decreased excretion. Lithium poisoning causes impaired renal function, drug interactions, volume depletion, and concurrent illnesses such as congestive heart failure or cirrhosis.[1,2] Lithium exerts its effects on a wide range of cellular functions by inhibiting inositol production, affects the protein kinase C signaling pathway, and inhibits glycogen synthase kinase 3 (GSK3).[ 3] Early recognition and management of lithium-induced organ toxicity can save lives and reduce significant morbidity
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