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Objective To explore the mitochondria and microsome of testis cells caused by nickel sulfate in rate.

目的从氧化应激角度探讨硫酸镍(NiSO4)对大鼠睾丸细胞线粒体及微粒体的毒性作用。

Abstract摘要: Objective To explore the mitochondria and microsome of testis cells caused by nickel sulfate in rate.

摘要摘要:目的从氧化应激角度探索硫酸镍(NiSO4)对大鼠睾丸细胞线粒体及微粒体的毒性功能。

Methods: Liver microsome was preparated from normal rat and human liver, which was to he treated with a series of concentrations of CsA or coadministration with Flu or MP. The activities of CYP3A in the microsomes were detected by using erythromycin as substrate.

製备大鼠和人肝微粒体,用不同浓度的CsA作用、加或不加MP、Flu,以红霉素为底物,经过NADPH系统孵育后,利用分光光度法测定人和大鼠肝微粒体的红霉素N-脱甲基酶活性。

To identify the location of Pfdyn, Triton X-100 and Biotin were used to extract different cell components'proteins.

在培养三周后出现了可以抗WR99210的含稳定pHD22y-Pfdyn微粒体的恶性疟原虫的克隆。

Methods: Liver microsome was preparated from normal rat and human liver, which was to he treated with a series of concentrations of CsA or coadministration with Flu or MP. The activities of CYP3A in the microsomes were detected by using erythromycin as substrate.

制备大鼠和人肝微粒体,用不同浓度的CsA作用、加或不加MP、Flu,以红霉素为底物,经过NADPH系统孵育后,利用分光光度法测定人和大鼠肝微粒体的红霉素N-脱甲基酶活性。

Alcohol, the most common cause, is a hepatotoxin that interferes with mitochondrial and microsomal function in hepatocytes , leading to an accumulation of lipid.

酒精,是最常见的原因,酒精所产生的毒素干扰了肝细胞线粒体和微粒体的功能,从而导致了大量脂肪酸的堆积。

Alcohol, the most common cause, is a hepatotoxin that interferes with mitochondrial and microsomal function in hepatocytes, leading to an accumulation of lipid.

乙醇是最常见的病因,作为肝毒素能阻碍肝细胞内的线粒体和微粒体的功能,导致脂质沉集。

At concentration of 2% PEG8000, 30% microsomal protein containing 10% of total P450 was precipitated. At concentration of 5% PEG8000, 55% microsomal protein containing 20% of total P450 was precipitated. At concentration of 8% PEG8000, 78% microsomal protein containing 30% of total P450 was precipitated. At concentration of 11% PEG8000, 85% microsomal protein containing 70% of total P450 was precipitated.

当PEG的浓度为2%时,约30%的微粒体蛋白和10%的P450被沉淀;PEG为5%时,约55%的微粒体蛋白和20%的P450被沉淀;PEG为8%时,约78%的微粒体蛋白和30%的P450被沉淀;PEG为11%时,约85%的微粒体蛋白和70%的P450被沉淀。

Methods Fe2+VitCinduced lipid peroxidation damage models were established by rat liver microsomes extraction. The expressions of malondialdehyde and superoxide dismutase were tested.

通过大鼠肝微粒体的提取,制备Fe2+VitC系统诱导的脂质过氧化损伤模型,检测车前子多糖对丙二醛的抑制作用以及对超氧化物歧化酶活性的影响,观察车前子多糖的抗脂质过氧化作用。

Results As shown in Western blot analysis, the presence of microsomes did not alter the molecular weight of TM-TNF , but it did result in the cleavage of the IL-2 signal peptide from S-TNFm,suggesting that the leader sequence of TNF might differ from the signal peptide of typical secretory protein in that it seemed not to have undergone cleavage during translation in the rough-faced endoplasmic reticulum.

结果 经Western blot 分析结果表明:微粒体的存在并不改变26×103 TM-TNF的分子量,但微粒体的存在能将S-TNFm上的IL-2信号肽切除,证实TNF引导序列与一般分泌性蛋白的&信号肽&不同,在粗面内质网翻译过程中不被切除。

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