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硒拮抗氟对肾脏损害的酶组织化学观察 被引量:1

ENZYME HISTOCHEMICAL OBSERVATION OF ANTAGONISM OF SELENIUM ON KIDNEY DAMAGE INDUCED BY FLUORINE
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摘要 本实验以酶组织化学方法(SDH、LDH、ACP、ALP)探讨硒对氟引起肾脏损害的拮抗作用。大鼠分为六组,A组常规饮水;B组饮水含亚硒酸钠2mg/L;C组饮水中含氟化钠150mg/L;D、E、F组饮水中分别含氟化钠150mg/L,依次含亚硒酸钠0.5mg/L、2mg/L、4mg/L。8周后断头处死,观察肾脏组织中SDH、LDH、ACP、ALP的活性。结果表明,与A组相比,C组近曲小管SDH、ALP活性减弱,LDH、ACP活性明显增加;B组SDH、ACP活性正常,基底膜清晰;D、E、F组均能提高SDH活性,其中E组较稳定;F组ACP活性较高。结果说明了氟引起肾近曲小管溶酶体的破坏,而硒(2mg/L)能稳定溶酶体膜。 To study the antagonism of selenium on kidney damage induced by Fluoride, rats were divided into six groups. Group A drank water as usual; Group B was given water containing Na 2SeO 3 2mg/L; Group C took water including NaF 150 mg/L; Group D, E, F drank water that contained NaF 150 mg/L and Na 2SeO 3 0 5 mg/L, 2 mg/L, 4 mg/L respectively. 8 weeks later, the rats were decapitated and the activities of SDH, LDH, ACP, ALP in kidney were measured by histochemical methods. The results were as follows: Compared with group A, the activities of SDH, ALP in proximal convoluted tubules were reduced, and the activities of LDH, ACP were obviously increased in group C; the activity of SDH was increased in group D, E, F, it is statle in group E and the activity of ACP was at high level in group F. It was suggested that Fluotide could induce the kidney damage by destroying the membrane of lysosom, and Se (2 mg/L) could protect the normal functions of renal tubules by stabilizing lysosom membrane.
出处 《中国组织化学与细胞化学杂志》 CAS CSCD 1999年第1期57-60,129,共5页 Chinese Journal of Histochemistry and Cytochemistry
关键词 肾脏 酶组织化学 大鼠 Selenium \ Fluoride \ Kidney \ Enzyme Rat
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  • 1李幼阳,安伶,孔可,王阿力,和晓青,陈积梅.肿瘤坏死因子对肾小球的损害作用[J].临床荟萃,1997,12(3):128-128. 被引量:2
  • 2KARADEMIR S, AKCAM M, KUYBULU A E, et al. Effects of fluorosis on QT dispersion, heart rate variability and echocardiographic parameters in chil dren [J]. Anadolu Kardiyol Der, 2011, 11 (2): 150-155.
  • 3SUN Z, NIU R, SU K, et al. Effects of sodium flu oride on hyperactivation and Ca^2+ signaling pathway in sperm from mice an in vivo study[J]. Arch Toxicol, 2010, 84(5): 353-361.
  • 4BARBIER O, ARREOI.A MENDOZA L, DEL RAZO L M. Molecular mechanism of fluoride toxicity [J]. Chem Biol Interact, 2010, 7(11): 319-333.
  • 5TSUNODA M, AIZAWA Y, NAKANO K, et al. Changes in fluoride levels in the liver, kidney, and brain [J]. Fluoride, 38(4):284-294.
  • 6MEHTA R L, KELLUM J A, SHAH S V, et al. Acute kidney injury network; report of an initiative to improve outcomes in acute kidney injury [J]. Crit Care, 2007, 11(2): 31.
  • 7WANG J M, NIU R Y, SUN Z L, et al. Effect of protein and calcium supplementation on bone metabolism and thyroid function in protein and calcium deficient rabbits exposed to fluoride[J]. Fluoride, 2008, 41(4): 307-315.
  • 8MIKLOS Z, KURTHY M, DEGRELL P, et al. Ischaemic postconditioning reduces serum and tubular tnf-α expression in ischaemic reperfused kidney in healthy rats [J]. Clin Hemorheol Micro, 2012, 50 (3) :167-178.
  • 9ZHAN X A,WANG M, XU Z R, et al. Toxic effects of fluoride on kidney function and histological structure in young pigs [J]. Fluoride, 2006, 39(1); 22-26.
  • 10BARONE J M, ALPONTI R F, FREZZATTI R. Differential efficiency of simvastatin and lipoic acid treatments on bothrops jararaca envenomation induced acute kidney injury in mice [J]. Toxicon, 2011, 57 (1) : 148-156.

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