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首页> 外文期刊>Journal of biochemical and molecular toxicology >Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats.
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Prophylactic effect of melatonin on lead-induced inhibition of heme biosynthesis and deterioration of antioxidant systems in male rats.

机译：褪黑素对血液生物合成铅诱导血液生物合成抑制的预防作用及雄性大鼠抗氧化体系的恶化。

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We studied the protective role of the pineal hormone melatonin on lead-induced suppression of the heme synthesis pathway as a consequence of reduced antioxidant systems in rat. We injected rats intramuscularly with lead acetate (10 mg/kg body weight) daily for 7 days, which significantly abolished heme synthesis as evidenced by decreased blood hemoglobin, liver delta-aminolevulinic acid synthetase, erythrocytic delta-aminolevulinic acid dehydratase, and hepatic iron content. These effects were accompanied with marked elevation of hepatic lipid peroxidation and decreased enzymatic antioxidants such as glutathione reductase, glutathione-S-transferase, superoxide dismutase, and catalase, as well as nonenzymatic antioxidants such as total sulfhydryl groups and glutathione. Furthermore, lead treatment caused hepatic deficiency in copper and zinc accompanied by a significant elevation of lead concentration in both plasma and liver. Daily pretreatment with melatonin (30 mg/kg body weight) intragastrically prevented the suppressive effects of lead on heme-synthesizing enzymes and iron deficiency. In addition, preadministration of melatonin reduced the inhibitory effect of lead on both enzymatic and nonenzymatic antioxidants. This was accompanied by marked normalization of lipid peroxidation and modulation of copper and zinc levels in liver. The action of melatonin on lead-induced changes was attributed to protection of the antioxidant capacity in cells in addition to the ability of melatonin to scavenge free radicals.
机译：我们研究了松果激素褪黑素对血红素合成途径的铅诱导抑制的保护作用，因为大鼠的抗氧化系统降低。我们每天用铅醋酸铅（10mg / kg体重）注射大鼠7天，这显着消除了血红素合成，如血液血红蛋白，肝δ-氨基乙酰丙烯酸合成酶，红细胞δ-氨基乙酸脱水酸脱氢酶和肝脏铁含量所证明。这些效果伴随着肝脂过氧化的标记升高，降低酶促抗氧化剂，如谷胱甘肽还原酶，谷胱甘肽-S-转移酶，超氧化物歧化酶和过氧化锆酶，以及非酶抗氧化剂，例如总巯基和谷胱甘肽。此外，铅治疗引起铜和锌中肝脏缺乏，伴随着血浆和肝脏中铅浓度的显着升高。每日预处理褪黑激素（30mg / kg体重）胃内阻止铅对血红素合成酶和缺铁的抑制作用。此外，褪黑素的较普拉替素降低了铅对酶和非酶抗氧化剂的抑制作用。这伴随着肝脏血液过氧化和铜和锌水平的标记标记。褪黑素对铅诱导的变化的作用归因于除褪黑素清除自由基的能力外，还归因于保护细胞中的抗氧化能力。

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