Isoniazid-rifampicin induced lipid changes in rats

Area of Science:

• Pharmacology
• Hepatology
• Biochemistry

Background:

• Tuberculosis treatment relies on isoniazid (INH) and rifampicine (RIF), effective but associated with potential hepatotoxicity.
• Altered lipid metabolism in the liver and serum may contribute to drug-induced liver injury.
• This study investigated the impact of INH-RIF on lipid profiles in a rat model.

Purpose of the Study:

• To examine the effects of isoniazid-rifampicine (INH-RIF) on hepatic marker enzymes and lipid profiles in rat serum and liver.
• To elucidate the role of lipid alterations in the pathogenesis of INH-RIF induced hepatotoxicity.

Main Methods:

• A rat model was used to induce hepatotoxicity with daily oral administration of INH-RIF (50 mg/kg each) for 28 days.
• Hepatic marker enzymes, total lipids, cholesterol, triglycerides, and phospholipids were measured in serum and liver.
• Standard biochemical assays were employed to quantify lipid fractions and enzyme activities.

Main Results:

• INH-RIF treatment significantly elevated hepatic marker enzymes, serum cholesterol, and total lipids.
• Liver triglycerides were significantly increased, while liver phospholipids were significantly decreased.
• Serum triglyceride and phospholipid levels showed no significant changes compared to the control group.

Conclusions:

• Isoniazid-rifampicine administration induces significant alterations in both serum and hepatic lipid profiles in rats.
• These observed lipid changes are strongly implicated in the mechanism of INH-RIF induced hepatotoxicity.
• Understanding these lipid alterations provides insight into managing tuberculosis drug-induced liver injury.