Kato A, Hishida A, Nakajima T
First Department of Medicine, Hamamatsu University School of Medicine, Japan.
Free Radic Biol Med. 1994 Jun;16(6):855-9. doi: 10.1016/0891-5849(94)90204-6.
Study was made to determine whether oxygen free radicals mediate uranium-induced acute renal failure (ARF). Superoxide dismutase (SOD), a superoxide anion scavenger, did not prevent uranium acetate (UA) (5 mg/kg, i.v.)-induced renal injury 48 h after injection. In contrast, dimethylthiourea (DMTU), a hydroxyl radical scavenger, significantly attenuated UA-induced rise in serum creatinine concentration (1.11 +/- 0.05 (DMTU) vs. 1.40 +/- 0.06 mg/dl (control), p < .05), and tubular necrosis. Dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, decreased UA-induced tubular damage. UA injection caused no increase in renal cortical malondialdehyde (MDA) content. DMTU and DMSO did not modify intrarenal MDA content. UA administration brought about significant increase in plasma renin activity but not in renal cortical renin content. Treatment with DMTU and DMSO had no effect on plasma renin activity or intrarenal renin content. It follows from these findings that DMTU and DMSO may attenuate UA-induced renal injury. Such a protective effect would not be mediated through modulation of lipid peroxidation or renin activity.
开展了一项研究以确定氧自由基是否介导铀诱导的急性肾衰竭(ARF)。超氧化物歧化酶(SOD),一种超氧阴离子清除剂,在注射醋酸铀(UA)(5毫克/千克,静脉注射)48小时后并不能预防肾损伤。相比之下,羟自由基清除剂二甲硫脲(DMTU)显著减轻了UA诱导的血清肌酐浓度升高(1.11±0.05(DMTU)对1.40±0.06毫克/分升(对照),p<0.05)以及肾小管坏死。羟自由基清除剂二甲基亚砜(DMSO)减轻了UA诱导的肾小管损伤。注射UA并未导致肾皮质丙二醛(MDA)含量增加。DMTU和DMSO并未改变肾内MDA含量。给予UA导致血浆肾素活性显著增加,但肾皮质肾素含量未增加。用DMTU和DMSO治疗对血浆肾素活性或肾内肾素含量没有影响。从这些发现可以得出,DMTU和DMSO可能减轻UA诱导的肾损伤。这种保护作用不会通过调节脂质过氧化或肾素活性来介导。