Abstract
Background: This study investigated selenium nanoparticles’ protective effects (SE-NPs) against carbon tetrachloride (CCl4)-induced hepatic injury in rats. Methods: Rats were divided into four groups (n = 8). Group 1 rats received the vehicle solution only. Group 2 received a single intraperitoneal injection of 1 mL/kg CCl4 in liquid paraffin (1:1 v/v). Group 3 was treated with SE-NPs (2.5 mg/kg) twice a week for three weeks before receiving CCl4 challenge. Oxidative stress, liver function, liver histopathology and serum lipid levels were evaluated. Results: Plasma concentrations of aspartate transaminase (AST), gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), urea, creatinine, malondialdehyde (MDA) and the toxicity marker, lactate dehydrogenase (LDH), were significantly elevated in rats treated with CCl4 compared to the controls. CCl4 also caused a significant decline in liver glutathione (GSH) concentration. SE-NP pretreatment significantly improved the level of AST, urea, creatinine, MDA, LDH, and GSH in the CCl4-injected rats towards the control levels. Conclusions: SE-NPs restored both liver function and hepatic structure in CCl4 treated rats. SE-NPs exhibit an ability to counter markers of liver injury induced by CCl4 and restore oxidative stability to lipid profiles and liver structure and function.
Highlights
CCl4 toxicity is mediated by metabolites that react with antioxidant enzymes [5]
This study is to investigate the effectiveness of selenium nanoparticles’ protective effects (SE-NPs) in protection against CCl4 induced hepatotoxicity
Our findings show that administration of SE-NPs significantly counters hepatotoxicity caused by CCl4, which might be due to antioxidant activity
Summary
Liver damage or hepatotoxicity is one of the most common side effects of any chemical drug or medicine-based treatment. It can be caused by herbal medicines [1], chemicals, metabolic intermediates and viruses. Chemical-induced liver toxicity is attributed to the classical mechanism, including apoptosis along with an upsurge in cytokine concentration and oxidative stress [2]. CCl4 toxicity is mediated by metabolites that react with antioxidant enzymes [5]. It raises the extent of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 β (IL-1β), nuclear factor (NF-κB). It is well established that CCl4 elicits free radicals and causes macrophages’
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