Kalapos M P, Littauer A, de Groot H
Klinische Forschergruppe Leberschädigung, Heinrich-Heine-Universität Düsseldorf, Germany.
Arch Toxicol. 1993;67(5):369-72. doi: 10.1007/BF01973710.
The toxicity of methylglyoxal and its ability to generate reactive oxygen species were investigated in cultured rat hepatocytes. Under aerobic and anaerobic conditions methylglyoxal increased lactate dehydrogenase (LDH) release and trypan blue uptake in a concentration dependent manner. Those concentrations of methylglyoxal causing cell injury (1 mM <) also caused the release of reactive oxygen species as indicated by peroxidase-catalyzed luminol chemiluminescence. Release of reactive oxygen was detectable only under aerobic conditions, and only became significant when a large portion of the cells had already lost their viability. It is concluded that methylglyoxal injuries cultured rat hepatocytes and induces the generation of reactive oxygen species. The reactive oxygen species, however, are essentially not involved in methylglyoxal hepatotoxicity but are released by already severely injured cells.
在培养的大鼠肝细胞中研究了甲基乙二醛的毒性及其产生活性氧的能力。在需氧和厌氧条件下,甲基乙二醛以浓度依赖性方式增加乳酸脱氢酶(LDH)释放和台盼蓝摄取。导致细胞损伤的甲基乙二醛浓度(>1 mM)也会导致活性氧的释放,如过氧化物酶催化的鲁米诺化学发光所示。活性氧的释放仅在需氧条件下可检测到,并且只有当大部分细胞已经失去活力时才变得显著。结论是甲基乙二醛损伤培养的大鼠肝细胞并诱导活性氧的产生。然而,活性氧基本上不参与甲基乙二醛的肝毒性,而是由已经严重受损的细胞释放。