Histological Evaluation of L-Carnitine’s Ability to Restore Liver Architecture Following Ceftriaxone Toxicity

Abstract

Background: Ceftriaxone, a commonly administered third-generation cephalosporin antibiotic, is generally regarded as safe but has been linked to few cases of hepatotoxicity. L-carnitine, a naturally occurring molecule, demonstrates significant antioxidant properties and indicates a potential hepatoprotective function.
Objective: This study aimed at establishing the hepatotoxicity of ceftriaxone in a rat model and the hepatoprotective effects of L-carnitine to counter the effects of the drug in causing hepatic damage. Methods: Forty adult male Wistar rats between 225 and 250 g weight were randomly stratified into four homogeneous groups (group n= 10): the untreated control, Group1 receiving ceftriaxone 250 1 kg/day -1 alone, Group2 receiving ceftriaxone 250 1 kg/day -1 at the same time receiving L-Carnitine 600 1 kg/day -1 at the same time, and Group3 receiving L-Carnitine 60 Treatments were delivered on a daily basis for a duration of 30 days. Hepatotoxicity was evaluated by quantifying serum concentrations of liver enzymes (AST, ALT, ALP), total serum bilirubin (TSB), and the muscle enzyme CPK. Histological changes of liver were conducted utilizing Hematoxylin & Eosin staining.
Results: Group 1 in the first cohort had severe histopathological changes characterized by hepatic toxicity induced by ceftriaxone treatment with the statistically significant increase (p< 0.05) of all the biochemical parameters compared the control. These hepatotoxic changes were significantly mitigated by the concomitant administration of L -carnitine with ceftriaxone (Group 2). Its safety was confirmed by the biochemical profile of the L-carnitine alone (G3) group, which was similar to that of the healthy control group.
Conclusion: that ceftriaxone causes considerable biochemical changes and hepatotoxicity in rats, predominantly via an oxidative stress mechanism. L-Carnitine demonstrates a substantial and significant protective effect against hepatotoxicity and associated histological structural damage.