硒,锌,钼对汞所致肝组织脂质过氧化保护作用的比较

硒、锌、钼对汞所致肝组织脂质过氧化保护作用的比较连祥霖林嗣豪已有实验表明，汞能诱发机体明显的脂质过氧化作用［１］，还有报道锌和钼能拮抗汞的毒性［２，３］，然而未见有关亚硒酸钠、硫酸锌、钼酸钠对汞所致脂质过氧化作用的影响。我们比较观察了亚硒酸钠、硫酸锌...     

硒和大蒜素对糖尿病小鼠心脏抗氧化功能及血液成分的保护作用

目的：观察亚硒酸钠,大蒜素及其合并用药对糖尿病小鼠心脏抗氧化功能及血液成分改变的保护作用。方法;以四氧嘧啶糖尿病小鼠动物模型,测定心脏抗氧化酶,脂质过氧化产物,一氧化氮（ＮＯ）和血液成分的含量。结果：糖尿病小鼠心脏抗氧化功能明显下降,ＮＯ含量明显减少,血液中白细胞数及血红蛋白含量明显下降,胆固醇含量明显升高;与糖尿病模型组小鼠相比,硒,大蒜素能明显逆转上述变化,其中硒对谷胱甘肽过氧化物酶活性的作用     

2(3)-叔丁基-4-羟基茴香醚对阿霉素诱发小鼠毒性的保护作用及其抗氧化机制

探讨叔丁基羟基茴香醚（ＢＨＡ）对阿霉素诱发小鼠毒性的保护作用及其机制。测定一些酶的活性及ＭＤＡ含量，并计数小鼠死亡率。结果经ＢＨＡ预处理后小鼠血清ＧＰＴ，ＧＯＴ，ＬＤＨ和ＣＫ活性及死亡率与阿霉素组比较均显著降低，并能显著降低由阿霉素所致ＭＤＡ含量升高的作用，同时ＢＨＡ对心肌及肝组织醌还原酶、ＧＳＴｓ和谷胱甘肽还原酶活性诱导增高。提示ＢＨＡ对阿霉素的毒性具有良好的保护作用，其作用途径可能与ＢＨＡ诱导抗氧化酶活性增加并抑制脂质过氧化反应有关     

云芝多糖对小鼠心、肝、脾、肾和红细胞抗氧化能力的影响

通过测定小鼠心、肝、脾、肾组织和红细胞脂质过氧化物含量和硒谷胱甘肽过氧化物酶活性，观察了云芝多糖对机体各组织及红细胞抗氧化能力的影响。结果表明，云芝多糖能提高机体各组织的硒谷胱甘肽过氧化物酶活性及降低脂质过氧化物含量，提示云芝多糖能有效地提高机体抗氧化能力，为防止或减轻脂质过氧化损伤提供了实验依据。     

依布硒啉对阿霉素引起的心脏脂质过氧化损伤的保护作用

依布硒琳（Ｅｂｓ）是一种具有过氧化物酶样活性的含硒有机化合物，本文以阿霉素处理的ＢＡＬＢ／ｃ小鼠为模型研究了Ｅｂｓ的保护作用．结果表明Ｅｂｓ能够减少阿霉素诱发的心肌脂质过氧化物的形成并提高机体谷胱甘肽过氧化物酶与脂质过氧化物的比值，防止阿霉素对心脏脂质过氧化损伤的毒性；同时测定血清肌酸激酶和谷草转氨酶活性，发现Ｅｂｓ也能保护组织免受阿霉素的损伤．     

丹皮总甙对化学性肝损伤保护作用机制

目的 研究丹皮总苷（ＴＧＭ）对ＣＣｌ４和Ｄ－Ｇａｌ－Ｎ致小鼠化学性肝损伤的保护作用机制。方法 采用ＣＣｌ４和Ｄ－Ｇａｌ－Ｎ所致小鼠化学性肝损伤模型进行研究,用ＴＢＡ法和ＤＴＮＢ法测定ＭＤＡ和ＧＳＨ－Ｐｘ。结果 ＴＧＭ具有促进肝脏糖原合成和提高血清蛋白含量的作用（Ｐ〈０．０１）,可明显降低肝匀浆脂质过氧化产物丙二醛（ＭＤＡ）的含量（Ｐ〈０．０１）及提高血清和肝脏谷胱甘肽过氧化物酶活力（Ｐ〈０．０１）     

葡萄糖酸锌对小鼠顺铂半数致死量及体内谷胱甘肽含量的影响

观察了葡萄糖酸锌（ＺＧ）对小鼠顺铂（ＣＤＤＰ）半数致死量和顺铂引起的谷胱甘肽（ＧＳＨ）含量变化的影响。结果表明：ＺＧ明显提高顺铂的半数致死量（１１．９３～１５．６５ｍｇ·ｋｇ－１）（Ｐ＜０．０５），同时ＺＧ还能增加给予ＣＤＤＰ的小鼠血中ＧＳＨ含量，降低血和肾组织中脂质过氧化物（ＬＰＯ）的含量，提示：ＺＧ对顺铂的毒性具有防护作用，其可能机制就是改善体内巯基化合物的代谢，抑制脂质过氧化反应。     

硒对过氧化氢所致老龄大鼠红细胞溶血及脂质过氧化的影响

本实验给老龄Wistar雄性大鼠腹腔注射亚硒酸钠(30μg/kg)15d,观察硒对过氧化氢所致红细胞溶血及脂质过氧化的抑制作用。结果表明硒降低了过氧化氢对红细胞的溶血率,同时过氧化氢所致脂质过氧化作用明显减弱。     

硒和大蒜素对糖尿病小鼠肝脏生化功能改变的保护作用

目的：观察亚硒酸钠、大蒜素及其合并用药对糖尿病小鼠肝脏生化功能改变的保护作用。方法：建立四氧嘧啶糖尿病小鼠动物模型，测定肝脏抗氧化酶、ATP酶活性、脂质过氧化产物、一氧化氮（NO）和肝糖原含量。结果：糖尿病小鼠肝脏抗氧化功能和Na^2 ,K^ -ATPase的活性明显下降，NO和肝糖原含量明显减少，与糖尿病模型组小鼠相比，硒、大蒜素能明显逆转上述变化，其中硒对GSHpx,Na^ ,K^ -ATPase,Ca^2 -ATPase活性的作用强于大蒜素，大蒜素对SOD活性的影响较大；硒、大蒜素合并用药较单独用药作用减弱。结论：硒、大蒜素对糖尿病小鼠肝脏具有良好的保护作用，两药合用作用减弱。     

芸香甙抗氧化作用的初步研究

芸香甙（Ｒｕ）是黄酮类化合物，本文就其抗氧化作用进行研究。在兔ＲＢＣ体外温育自氧化试验中，３．２×１０－５ｍｏｌ·Ｌ－１Ｒｕ可显著抑制ＲＢＣ自氧化．并可减少ＲＢＣ自氧化过程中脂质过氧化产物──ＭＤＡ的含量．说明ＲＵ对ＲＢＣ的自氧化溶血损伤有一定的保护作用，并可能与抑制脂质过氧化反应有关；灌胃Ｒｕ２０～８０ｍｇ·ｋｇ－１不仅可显著减少小鼠血浆中ＭＤＡ含量，也可显著提高大鼠血浆中ＳＯＤ活性，并有一定的量效关系，结果进一步提示ＲＵ抗脂质过氧化作用可能与提高ＳＯＤ活性有关。     

Simultaneous administration of sodium selenite and mercuric chloride decreases efficacy of DMSA and DMPS in mercury elimination in rats

Two chelating agents meso-2,3-dimercaptosuccinic acid (DMSA) and sodium 2,3-dimercapto-propane-1-sulphonate (DMPS) were tested for their efficiency in mercury removal from the body of rats in the presence and in the absence of selenium. Female Wistar rats were given a single intraperitoneal injection of mercuric chloride or an equimolar mixture of mercuric chloride and sodium selenite (1.5 micromol/kg body weight). The chelating agents were given orally, in excess (500 micromol DMSA/kg body weight; 300 micromol DMPS/kg body weight), 30 min after the administration of mercury and selenium. The animals were euthanized 24 h after the treatment and mercury in the kidney, liver, and 24 h urine was determined using cold vapour atomic absorption spectrometry (CV-AAS). The simultaneous administration of mercuric chloride and sodium selenite led to a redistribution of mercury in the organs, so that accumulation of mercury in the kidneys was decreased and in the liver increased. Selenite also caused decrease in the level of urinary mercury excretion. Both chelating agents were effective in mercury removal from the body, by increasing its urinary excretion. However, when animals were simultaneously treated with mercury and selenite, the rise of mercury excreted in the urine due to the treatment with chelating agents was lower when compared to animals receiving mercury without selenite. It is concluded that sodium selenite decreases the efficiency of DMSA and DMPS in mercury removal from the body of rats.     

Changes in distribution of mercury and selenium in soluble fractions of rabbit tissues after simultaneous administration

The existing states of mercury and selenium in the blood and in soluble fractions of perfused rabbit liver and kidney were studied by gel filtration on Sephadex G-200 1 hr or 24 hr after intravenous injection of mercuric chloride and/or sodium selenite. Both mercury and selenium in the plasma and stroma-free hemolysate were found to exist in the high-molecular weight fraction following simultaneous injection of mercuric chloride and sodium selenite. Patterns in gel filtration of the plasma and the stroma-free hemolysate did not show any significant change between 1 hr and 24 hr after the administration. A similar tendency as described above was obtained with the liver-soluble fraction at 24 hr after injection of mercuric chloride and sodium selenite. A possible role of the high-molecular weight complex, which is quickly formed by the interaction of mercury and selenium in blood stream, in decreasing the acute renal toxicity of inorganic mercury is discussed.     

Effects of selenium on toxicity and ultrastructural localization of mercury in cultured murine macrophages

The effects of selenium on cellular toxicity and histochemical distribution of mercury were examined in a cell culture system of mouse peritoneal macrophages. Selenium protected against the toxicity of mercury in cultures exposed to 4 microM of mercuric chloride. Selenomethionine caused a significant increase in cell survival throughout the experiments, while sodium selenite delayed the toxicity of mercury for a while, after which selenite itself had a toxic effect. The amount of mercury visualized by autometallography was increased in macrophage cultures pre-exposed to sodium selenite or selenomethionine. The additional mercury made visible by this histochemical demonstration was located in the cytoplasm as well as in the lysosomes.     

Hemolytic Effects of Sodium Selenite and Mercuric Chloride in Human Blood

Many works have reported the interaction between selenium and mercury in the mammalian body and that chalcogen seems to have a protective effect against mercury toxicity. The aim of this study was to investigate the hemolytic effects of sodium selenite and/or mercuric chloride in human blood under in vitro conditions. For this, total venous blood from healthy subjects (males and females) was heparinized and incubated at 37°C for 90 min with different concentrations of sodium selenite and/or mercuric chloride. The hemolytic effects of compounds were evaluated by measuring plasma hemoglobin concentration after centrifugation. In addition, 2-thiobarbituric acid reactive substances (TBARS) from plasma and erythrocytes, as well as erythrocyte nonprotein thiols (NPSH), were also evaluated in order to investigate molecular mechanisms related to selenite- or mercury-induced hemolysis. Mercuric chloride and sodium selenite, alone (400 µM), promoted a small in vitro hemolytic effect in human erythrocytes. However, when blood was exposed to both compounds (200 µM of each), there was an extremely high synergistic hemolytic effect. The exposure of blood to sodium selenite (400 µM), mercuric chloride (400 µM), and both compounds (200 µM each) did not alter erythrocyte TBARS levels. Sodium selenite presented a high oxidant effect toward erythrocyte NPSH; however, this effect was inhibited by mercuric chloride. The current results point to a synergistic hemolytic effect of sodium selenite and mercuric chloride in human blood, suggesting new understanding on the selenium–mercury antagonism. Moreover, this observed hemolysis seems to be not related to lipoperoxidation or thiol depletion.     

Spirulina fusiformis provides protection against mercuric chloride induced oxidative stress in Swiss albino mice

Oxidative stress induced by mercuric chloride (5 mg/kg body weight i.p.) in mice substantially increases the lipid peroxidation level along with corresponding decrease in the reduced glutathione and various antioxidant enzymes in liver and increase in serum transaminases activity. Supplementation of Spirulina (800 mg/kg body weight orally, in olive oil, along with mercuric chloride) for 40 days resulted in decreased LPO level, serum glutamate oxaloacetate and serum glutamate pyruvate transaminase activity along with increase in liver GSH level. The activities of antioxidants enzymes superoxide dismutase, catalase and glutathione-S-transferase were also concomitantly restored to near normal level by Spirulina supplementation to mercuric chloride intoxicated mice. The results clearly demonstrate that Spirulina treatment augments the antioxidants defense mechanism in mercuric chloride induced toxicity and provides evidence that it may have a therapeutic role in free radical mediated diseases.     

Hemolytic effects of sodium selenite and mercuric chloride in human blood

Many works have reported the interaction between selenium and mercury in the mammalian body and that chalcogen seems to have a protective effect against mercury toxicity. The aim of this study was to investigate the hemolytic effects of sodium selenite and/or mercuric chloride in human blood under in vitro conditions. For this, total venous blood from healthy subjects (males and females) was heparinized and incubated at 37 degrees C for 90 min with different concentrations of sodium selenite and/or mercuric chloride. The hemolytic effects of compounds were evaluated by measuring plasma hemoglobin concentration after centrifugation. In addition, 2-thiobarbituric acid reactive substances (TBARS) from plasma and erythrocytes, as well as erythrocyte nonprotein thiols (NPSH), were also evaluated in order to investigate molecular mechanisms related to selenite- or mercury-induced hemolysis. Mercuric chloride and sodium selenite, alone (400 microM), promoted a small in vitro hemolytic effect in human erythrocytes. However, when blood was exposed to both compounds (200 microM of each), there was an extremely high synergistic hemolytic effect. The exposure of blood to sodium selenite (400 microM), mercuric chloride (400 microM), and both compounds (200 microM each) did not alter erythrocyte TBARS levels. Sodium selenite presented a high oxidant effect toward erythrocyte NPSH; however, this effect was inhibited by mercuric chloride. The current results point to a synergistic hemolytic effect of sodium selenite and mercuric chloride in human blood, suggesting new understanding on the selenium-mercury antagonism. Moreover, this observed hemolysis seems to be not related to lipoperoxidation or thiol depletion.     

Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E

Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300–320 g and each group six animals) were given mercuric chloride (1 mg/kg bw) and/or sodium selenite (0.25 mg/kg bw) + vitamin E (100 mg/kg) daily via gavage for 4 weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.     

Ameliorative stroke of selenium against toxicological effects of mercuric chloride in liver of freshwater catfish Heteropneustes fossilis (Bloch)

Mercury, a prevalent and unrelenting toxin, occurs in a variety of forms in freshwater as well as, in marine life. Mercury is an important inducer of oxidative stress in fish leading to formation of reactive oxygen species. Selenium is an essential micronutrient for animals and has antagonistic effect against mercuric toxicity in fishes. Present study has been made to evaluate toxic effect of HgCl₂ (0.15 mg/L) on liver of freshwater catfish Heteropneustes fossilis (Bl.). Protective ability of selenium has been investigated by simultaneous exposure of fish with sodium selenite (0.15 mg/L) along with mercuric chloride. For present study Fishes were divided into three groups of ten fishes each the first group served as control, while the second group fish were exposed to HgCl₂. Animals of third group were treated with HgCl₂ and Na₂SeO₃. Results reveal that mercury induced lipid peroxidation and in response to this, antioxidants reduced glutathione (GSH) and Catalase (CAT) were reduced whereas, Glutathione reductase (GR) level was enhanced. These antioxidants scavenge the reactive oxygen radicals. Hg induced histopathological damage and elevation in alkaline phosphatase (ALP) and transaminases and reduction in protein and glucose contents were evidently seen in catfish liver. Intriguingly, results indicate that under stress of mercury, the fish actively generate oxidative stress and antioxidant responses, which can be used as biomarkers of pollution. Simultaneous exposure to Selenium along with Hg suppressed Hg uptake and lipid peroxidation. Histological architecture and all biochemical parameters were maintained near normal in the presence of selenium in liver of the catfish. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 927–936, 2015.     

二氧化硫吸入对小鼠脾脏的氧化应激作用

目的　研究不同浓度二氧化硫 (SO2 )吸入后雌、雄小鼠脾脏脂质过氧化水平和抗氧化能力的变化。方法　染毒组小鼠每日接受 4hSO2 吸入染毒 ,剂量分别为 2 8、5 6、112和 168mg m3,持续 7d。对照组接受新鲜空气。用硫代巴比妥酸 (TBARS)染色法测定丙二醛 (MDA)含量 ,分光光度法测定谷胱甘肽 (GSH)含量 ,二硫代双硝基苯甲酸 (DTNB)直接法测定谷胱甘肽过氧化物酶 (GSH Px)活力 ,改进的抗坏血酸 (Vc)终止法测定超氧化物歧化酶 (SOD)活力。结果　(1)随着SO2 吸入浓度增加 ,雌雄小鼠脾脏内MDA含量增加 ,GSH Px、SOD活力降低 ,在较高浓度 (>112mg m3)时 ,差异有显著性 (P <0 0 5 ) ;(2 ) 2 8mg m3SO2 吸入使GSH含量显著升高 (P <0 0 5 ) ,但在高浓度 (168mg m3)时 ,其含量却显著下降。 (3 )SO2 吸入对雌雄小鼠脾脏的氧化损伤作用没有性别差异。结论　SO2 吸入浓度高于 112mg m3以上时引起小鼠脾脏脂质过氧化作用增强 ,抗氧化能力降低 ,且存在一定的剂量依赖关系 ,提示较高浓度SO2 对脾的毒作用与诱发小鼠体内产生过量自由基有关     

硒多糖、亚砷酸钠对大鼠肝微粒体酶和GSH-Px等的影响

研究了硒多糖、亚砷酸钠在体内、外对大鼠肝微粒体酶细胞色素Ｐ－４５０、ｂ５、ＮＡＤ（Ｐ）Ｈ－细胞色素Ｃ还原酶、谷胱甘肽硫转移酶（ＧＳＴ）的影响;并通过测定硒多糖、亚砷酸钠对肝谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）和脂质过氧化（ＬＰＯ）的影响,探讨了硒、砷相互作用的机理。结果表明：连续７天腹腔注射０．２ｍｇ／ｋｇ硒多糖,细胞色素Ｐ－４５０、ｂ５的含量、ＧＳＴ的活性降低（Ｐ＜０．０５）;硒多糖明显诱导ＧＳＨ－Ｐｘ的活性,降低脂质过氧化,拮抗亚砷酸钠对ＬＰＯ的作用。亚砷酸钠显著增强肝细胞脂质过氧化（Ｐ＜０．０５）,对ＧＳＨ－Ｐｘ和肝微粒体酶无明显影响