Abstract
The present study was designed to investigate the dose-dependent protective effect of L-carnitine (LC) on thyroid hormone-induced oxidative stress in rat liver tissue. Twenty-one male Sprague Dawley rats were divided into four groups: control, hyperthyroidism, hyperthyroidism plus L-carnitine 100, and hyperthyroidism plus L-carnitine 500. Hyperthyroidism was induced in rats by injecting 250 μg of L-thyroxine/kg body weight/day for twenty consecutive days. The activities of catalase (CAT), glutathione peroxidase (GPX) and myeloperoxidase (MPO) and the level of malondialdehyde (MDA) were measured in liver homogenates. The liver CAT, GPX and MPO activities were significantly lower in the hyperthyroid rats than in the control group. Treating hyperthyroid rats with both low-dose (100 mg/kg) and high-dose (500 mg/kg) L-carnitine for 10 days resulted in a marked increase in the activities of the antioxidant enzymes in the liver tissue. The present study indicates that the low-dose L-carnitine application was sufficient to prevent L-thyroxine-induced oxidative stress in rat livers.
Highlights
Thyroid hormones are the most important factor involved in setting the basal metabolic rate in target tissues such as the liver, heart, kidney and brain
The liver CAT, glutathione peroxidase (GPX) and MPO activities were significantly lower in the hyperthyroid rats than in the control group
Treating hyperthyroid rats with both low-dose (100 mg/kg) and high-dose (500 mg/kg) L-carnitine for 10 days resulted in a marked increase in the activities of the antioxidant enzymes in the liver tissue
Summary
Thyroid hormones are the most important factor involved in setting the basal metabolic rate in target tissues such as the liver, heart, kidney and brain. Thyroid hormone administration to vertebrates leads to an accelerated basal metabolic rate and oxygen consumption in the target tissues [1]. Both clinical [2, 3] and experimental [1, 4, 5] studies have demonstrated that hyperthyroidism can cause an elevation in oxidative stress, most likely because of increased mitochondrial oxygen consumption. The superoxide (O2.-), hydroxyl (HO), perhydroxyl radicals (HO2-) and nitric oxide (NO) are the most important free radicals that are derived from oxygen [7].
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