Salovsky P, Shopova V, Dancheva V, Marev R
Department of Disaster Medicine, University of Medicine, Pleven, Bulgaria.
Hum Exp Toxicol. 1992 May;11(3):217-22. doi: 10.1177/096032719201100310.
One-hundred male white rats were given a single intratracheal dose of 0, 5 mg kg-1 cadmium acetate. There was a fall in catalase (CAT) and superoxide dismutase (SOD) in lung homogenate throughout the 30 d after treatment. Non-protein sulphhydryl (NPSH) content, glucose-6-phosphate dehydrogenase (G-6-PD) and glutathione peroxidase (GP) were all increased from days 5 to 15. There was an increase in lactate dehydrogenase (LDH) and protein in bronchoalveolar lavage fluid (BALF) and in the relative weight of the lungs which provide evidence of severe toxic lesions of the lungs. Increased lipid peroxidation provoked by the reduced lung antioxidant protective capacity may be an important mechanism in the pulmonary damage caused by cadmium.
给100只雄性白鼠经气管内一次性注射0、5毫克/千克的醋酸镉。在治疗后的30天内，肺匀浆中的过氧化氢酶（CAT）和超氧化物歧化酶（SOD）含量均下降。非蛋白巯基（NPSH）含量、葡萄糖-6-磷酸脱氢酶（G-6-PD）和谷胱甘肽过氧化物酶（GP）在第5天至第15天均升高。支气管肺泡灌洗液（BALF）中的乳酸脱氢酶（LDH）和蛋白质以及肺的相对重量增加，这为肺部严重毒性损伤提供了证据。肺抗氧化保护能力降低引发的脂质过氧化增加可能是镉导致肺损伤的重要机制。
