Abstract
It is known that the combined use of antibiotics, such as isoniazid and rifampicin, in the treatment of tuberculosis causes oxidative kidney damage. The aim of this study was to biochemically and histopathologically investigate the effect of lycopene on oxidative kidney damage due to the administration of isoniazid and rifampicin in albino Wistar male rats. Lycopene at a dose of 5 mg/kg was orally administered to lycopene+isoniazid+rifampicin (LIR) rats, and normal sunflower oil (0.5 mL) was orally administered to isoniazid+rifampicin (IR) and healthy control (HG) rats as vehicle by gavage. One hour after the administration of lycopene and vehicle, 50 mg/kg isoniazid and rifampicin were given orally to the LIR and IR groups. This procedure was performed once a day for 28 days. Rats were sacrificed by a high dose of anesthesia at the end of this period, and oxidant-antioxidant parameters were measured in the removed kidney tissues. Creatinine and blood urea nitrogen (BUN) levels were measured in blood samples, and kidney tissues were also evaluated histopathologically. The combined administration of isoniazid and rifampicin changed the oxidant-antioxidant balance in favor of oxidants, and it increased blood urea nitrogen and creatinine levels, which are indicators of kidney function. Co-administration of isoniazid and rifampicin also caused oxidative kidney damage. Lycopene biochemically and histopathologically decreased oxidative kidney damage induced by isoniazid and rifampicin administration. These results suggested that lycopene may be beneficial in the treatment of nephrotoxicity due to isoniazid and rifampicin administration.
Highlights
Tuberculosis caused by Mycobacterium affects the lungs and other vital organs of the body (1)
Biochemical findings Thiobarbituric acid reactive substances (TBARS) levels in the kidney tissues of animals treated with the isoniazid and rifampicin combination increased significantly compared to those of the healthy and lycopene groups (Po0.0001)
Isoniazid and rifampicin applied in combination to induce nephrotoxicity caused an increase in TBARS and total oxidant status (TOS) levels as well as a decrease in tGSH and total antioxidant status (TAS) levels in animal kidney tissues
Summary
Tuberculosis caused by Mycobacterium affects the lungs and other vital organs of the body (1). Tuberculosis is a treatable disease, it is a public health problem representing the second highest cause of mortality among communicable diseases globally (2). Antibiotics, such as isoniazid, rifampicin, pyrazinamide, ethambutol, and streptomycin, are used in the treatment of tuberculosis (3). It has been found that damage to kidney tissues is decreased by antioxidants, which decrease the end products of lipid peroxidation (LPO) such as malondialdehyde (MDA) (7). Together, these studies suggest that the use of antioxidants may be beneficial in the prophylaxis of kidney damage associated with the combined use of isoniazid and rifampicin
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