Korzh E V
Med Tr Prom Ekol. 1998(2):10-7.
In experimental pneumoconiosis both under normal and heating ambient temperature lipid peroxidation is not activated, although heating microclimate increases alteration of lung tissue and induces rapid and intensive pulmonary fibrosis. Association of dust and heating microclimate prolongs a period of "stress" myocardial affliction due to intensified lipid peroxidation and exhausted endogenous glutathione peroxidase, afterwards lipid peroxidation decreases with progressing sclerosis and fat degeneration in heart.
在实验性尘肺中，无论在正常环境温度还是加热环境温度下，脂质过氧化均未被激活，尽管热微气候会增加肺组织的改变并诱发快速且强烈的肺纤维化。粉尘与热微气候的共同作用会延长“应激”性心肌损伤的时期，这是由于脂质过氧化加剧和内源性谷胱甘肽过氧化物酶耗尽所致，随后随着心脏硬化和脂肪变性的进展，脂质过氧化会降低。
