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硒对氟致大鼠肾脏损伤保护作用的实验观察 被引量:4

Protective effect of selenium on fluoride-induced renal impairments in rats
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摘要 目的观察硒对氟致大鼠肾脏损伤的保护作用,探讨硒的最佳作用剂量及作用靶点。方法断乳SD雄性大鼠80只,按体质量随机分8组,每组10只。对照组饮用自来水;染氟组饮用50mg/L的氟化钠溶液;低、中、高硒组分别饮用0.375、0.750、1.500mg/L的亚硒酸钠溶液;氟+低、中、高硒组分别饮用50mg/L的氟化钠和0.375、0.750、1.500mg/L的亚硒酸钠两两组合的溶液。染毒6个月后,测大鼠肾脏组织的氧化水平和核因子KB(NF—κB)的表达量。结果染氟组大鼠体质量[(695.95±55.89)g]低于对照组[(782.69±56.12)g,P〈0.01],染氟组谷胱甘肽过氧化物酶(GSH—Px)活性[(55.86±5.09)U/mgprot]与对照组[(68.66±4.52)U/mgprot]比较,差异无统计学意义(P〉0.05),但有降低的趋势。染氟组大鼠总抗氧化能力(T—AOC)水平[(7.54±1.35)U/mgprot]低于对照组[(9.03±0.37)U/mgprot,P〈0.05],染氟组丙二醛(MDA)水平[(3.86±0.31)nmol/mgprot]高于对照组[(3.14±0.32)nmol/mgprot,P〈0.05]。氟+高硒组GSH—Px活性[(74.99±8.41)U/mgprot]高于染氟组[(55.86±5.09)U/mgprot,P〈0.05],MDA水平[(3.17±0.20)nmol/mgprot]低于染氟组[(3.86±0.31)nmol/mgprot,P〈0.05]。染氟组、高硒组和氟+低硒组的NF—KB的表达水平(0.360±0.015,0.367±0.007,0.376±0.006)高于对照组(0.312±0.022,P均〈0.05),氟+高硒组(0.312±0.005)低于染氟组(0.360±0.015,P〈0.05)。结论1.500mg/L硒是本实验条件下硒对慢性氟中毒致大鼠肾脏损伤的最佳保护作用剂量,NF—κB可能是硒拮抗氟中毒的药物靶点。 Objective To explore the protective effect of selenium, an antioxidant, on fluoride-induced renal injury in rats and find out the optimal level of selenium against fluoride toxicity and its valid molecular target. Methods All 80 male weanling SD rats were randomly divided into 8 groups by body weight as follows: normal control group(drinking tap water), fluoride exposed group (drinking water containing 50 mg/L ofNaF), low, middle, high selenium exposed groups(drinking water containing 0.375, 0.750, 1.500 mg/L of Na2SeO3) and low, middle, high Se-fluoride groups (drinking water containing both 50 mg/L NaF and three doses of Na2SeO3 as abovementioned, respectively). After 6 months, the rats were killed then the oxidation level and nuclear factor KB(NF-κB) expression level in kidney were measured. Results The weight of the fluoride exposed group [ (695.95 ± 55.89 )g 1 was significantly decreased than the controls [ (782.69 ± 56.12 ) g, P 〈 0.01 ]. Glutathione peroxidase (GSH-Px) activity of fluoride exposed group [ (55.86 ± 5.09) U/mgprot ] was not significantly different but decreased. Tatal antioxidant capacity (T-AOC) activity in fluoride exposed group [ (7.54 ± 1.35)U/mgprotl significantly decreased than the controls[ (9.03 ± 0.37) U/mgprot, P 〈 0.051. In addition, a significant increase of malondialdehyde (MDA) in fluoride exposed group [ (3.86 ± 0.31 )nmol/mgprot, P 〈 0.051 was observed than the controls [ (3.14 ± 0.32) nmol/mgprot, P 〈 0.05]. GSH-Px activity of high Se-fluoride group [ (74.99 ± 8.41 )U/mgprot] was significantly higher than the fluoride exposed group [ (55.86 ± 5.09)U/mgprot, P 〈 0.05 ] and its MDA level [ (3.17 ± 0.20) nmol/mgprot] was lower than the fluoride exposed group [ (3.86 ± 0.31) nmol/mgprot, P 〈 0.05]. NF-κB expression levels of fluoride group, high selenium group and low Se-fluoride group(0.360 ± 0.015,0.367 ± 0.007,0.376 ± 0.006, respecyively) were obviously increased compared with the controls(0.312 ± 0.022, P 〈 0.05); it was significantly lower in high Se-fluoride group(0.312 ± 0.005) than in fluoride exposed group(0.360 ± 0.015, P 〈 0.05). Conclusions Na2SeO3 of 1.5 mg/L is the optimal dose against chronic fluorosis on kidney injury under this experimental condition. NF-κB is likely to be a target molecule of the selenium as an antagonist on fluorosis.
出处 《中国地方病学杂志》 CAS CSCD 北大核心 2011年第2期137-141,共5页 Chinese Jouranl of Endemiology
基金 国家自然科学基金(30872195) 浙江省自然科学基金(Y2100431)
关键词 氟化物中毒 脂质过氧化作用 核因子-ΚB Selenium Fluoride poisoning Kidney Lipid peroxidation NF-kappa B
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