Institute of Biomedical Research, Branch of Federal Scientific Center "Vladikavkaz Scientific Center", Russian Academy of Sciences, Vladikavkaz, the Republic of North Ossetia - Alania, Russia.
Bull Exp Biol Med. 2022 Jun;173(2):205-209. doi: 10.1007/s10517-022-05519-x. Epub 2022 Jun 23.
In rats with lead intoxication (intramuscular administration of lead acetate in a dose 5 mg/kg for 30 days), the development of oxidative stress, reduced expression of endothelial NO synthase and total metabolites of NO production, as well as an increased content of norepinephrine were observed. Lead-induced nephropathy developed; diuresis and sodium excretion increased due to a decrease in tubular transport of water and sodium ions. Activation of free-radical reactions in cells of the renal cortex and medulla contributed to inhibition of Na,K-ATPase. LPO caused damage to cardiomyocytes, hepatocytes, which was seen from elevation of AST, ALT, γ-glutamyl transpeptidase, and alkaline phosphatase in the blood serum and a decrease in activity of Na,K-ATPase in the organs tissues. Metabolic disorders revealed in saturnism in experimental rats (LPO activation, reduced expression of endothelial NO synthase and total metabolites of NO, and increased blood norepinephrine) contributed to the development of vascular endothelial dysfunction and hemodynamics disturbances, and damage to cells of internal organs: kidney, myocardium, liver.
在铅中毒大鼠(肌肉内注射醋酸铅,剂量为 5mg/kg,持续 30 天)中,观察到氧化应激的发展、内皮型一氧化氮合酶和总一氧化氮产物表达减少,以及去甲肾上腺素含量增加。铅诱导的肾病发展;由于肾小管对水和钠离子的转运减少,利尿和钠排泄增加。自由基反应在肾皮质和髓质细胞中的激活导致 Na,K-ATP 酶抑制。LPO 导致心肌细胞、肝细胞损伤,这可从血清中天冬氨酸转氨酶、丙氨酸转氨酶、γ-谷氨酰转肽酶和碱性磷酸酶的升高以及器官组织中 Na,K-ATP 酶活性的降低看出。实验大鼠的铅中毒(LPO 激活、内皮型一氧化氮合酶和总一氧化氮产物表达减少,以及血液去甲肾上腺素增加)导致血管内皮功能障碍和血液动力学紊乱以及内部器官细胞损伤:肾脏、心肌、肝脏。