The protective effect of lycopene against oxidative kidney damage associated with combined use of isoniazid and rifampicin in rats.

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.

The protective effect of lycopene against oxidative kidney damage associated with combined use of isoniazid and rifampicin in rats

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.

Inferior pancreaticoduodenal artery false aneurysm: a rare cause of gastrointestinal bleeding diagnosed by three-dimensional computed tomography.

We report a 57-year-old man who presented with a two-month history of persistent epigastric pain associated with indigestion, weight loss and jaundice. Contrast-enhanced computed tomography revealed a large pseudoaneurysm 87 mm x 68 mm in diameter, with its origin from the inferior pancreaticoduodenal artery of the superior mesenteric artery and in continuity with an ectatic gastroduodenal artery. The aneurysmal mass exerted direct pressure over the head of the pancreas, common bile duct and duodenum, causing obstruction. Non-selective abdominal angiography confirmed the aneurysm stemming from the inferior pancreaticoduodenal artery. Because of the obstructive symptoms and the size of the aneurysm, surgery was planned, but the patient refused and died from massive gastrointestinal bleeding one month later.

Effects of trimetazidine on lipid peroxidation, antioxidant enzyme activities and plasma brain natriuretic peptide levels in patients with chronic cor pulmonale.

An oxidant/antioxidant imbalance in favour of oxidants appears to occur in chronic cor pulmonale (CCP). Oxidative stress could also be a critical event in the pathogenesis of this condition. Trimetazidine (TMZ) has antioxidant properties and may affect the utilization of oxygen radicals. We investigated the effect of TMZ (20 mg three times daily, orally) on activities of erythrocyte malondialdehyde (MDA) and catalase (eCAT), erythrocyte and plasma glutathione peroxidase (GSH-Px) and plasma superoxide dismutase (pSOD) in CCP patients. We also assessed changes in plasma levels of brain natriuretic peptide (BNP) with TMZ therapy. Sixty CCP patients with significantly higher MDA and markedly lower pSOD, eCAT and GSH-Px (erythrocyte) activities than 24 healthy controls were randomly allocated to receive routine treatment or routine treatment plus TMZ. After 3 months' therapy, greater pSOD, eCAT and GSH-Px (erythrocyte and plasma) activities and lower MDA activity were found with TMZ treatment compared with routine treatment. Plasma BNP levels were significantly lower in TMZ-treated patients and higher in the routine treatment group than in the control group. TMZ improved antioxidant levels, decreased oxidative stress and decreased plasma BNP levels in CCP patients.