Müller L
Toxicol Lett. 1983 Feb;15(2-3):159-65. doi: 10.1016/0378-4274(83)90210-2.
Isolated hepatocytes form thiobarbituric acid (TBA)-reactants, a parameter of lipid peroxidation (LPO), when exposed to cadmium (Cd). Paracetamol (Para) inhibits this response, dependent on time and concentration. Cd-induced SH-group decline, however, and enhanced plasma membrane permeability to Trypan Blue (TB) were not inhibited by Para. This indicates that Cd-induced cell damage and Cd-induced LPO are independent events. Experiments using cells with enhanced and lowered metabolism of Para after phenobarbital- and acetone- or heat-and metyrapone treatment, respectively, suggest a potentially inhibitory effect of both Para and its metabolite(s) on LPO. The antioxidative potency of Para turned out to be small compared to that of the radical scavenger (+)-cyanidanol-3.
分离的肝细胞在暴露于镉（Cd）时会形成硫代巴比妥酸（TBA）反应物，这是脂质过氧化（LPO）的一个参数。对乙酰氨基酚（扑热息痛，Para）可抑制这种反应，其抑制作用取决于时间和浓度。然而，镉诱导的巯基减少以及质膜对台盼蓝（TB）通透性的增加并未被扑热息痛抑制。这表明镉诱导的细胞损伤和镉诱导的脂质过氧化是独立事件。分别用苯巴比妥和丙酮处理或热和甲吡酮处理后，对乙酰氨基酚代谢增强和降低的细胞进行的实验表明，扑热息痛及其代谢产物对脂质过氧化可能具有抑制作用。结果表明，与自由基清除剂（+）-氰定醇-3相比，扑热息痛的抗氧化能力较小。
