Biochemical disturbances caused by ranitidine in rats: attention to bilirubin–lipids relation and benefits of capsiate

Abstract Ranitidine is an H2-receptor antagonist used to control acid disorders in the gastrointestinal tract. But the long-term use of ranitidine is related to liver dysfunction, which may alter bilirubin levels and disrupt lipid metabolism. Bilirubin, beyond being a liver function marker, plays a role against oxidative stress and lipid dysregulation. In this research, we set out to study the toxic outcomes of ranitidine in selected biochemical parameters with emphasis on the biochemical relationship between bilirubin dysregulation and lipid disturbances and to evaluate the therapeutic potential of capsiate in counteracting this disturbed relationship. The rats are grouped as follows: control, ranitidine-treated, capsiate-treated, and a combination of ranitidine with capsiate-treated group. Capsiate and ranitidine were orally given at doses of (60 mg/kg.b.wt and 300 mg/kg.b.wt, respectively). Body weight gain and liver weights and relative liver weights; serum levels of direct bilirubin, lipids, glucose, hematological parameters, electrolytes, and comet assay results were evaluated. Ranitidine causes metabolic disturbances, linked with bilirubin, lipids, and glucose regulation, and other biochemical assessments as well as genotoxicity. These findings give new insights about the biochemical link between bilirubin and lipid disturbances in ranitidine-induced liver alterations. On the other hand, capsiate mitigates the biochemical disturbances, genotoxicity, and modulate the disturbed relationship between bilirubin and lipids. The efficacy of capsiate to modulate these disturbances positions it as a promising candidate for future therapeutic applications. Graphical abstract