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首页> 外文期刊>Human and Experimental Toxicology >Alterations induced in vitro by ochratoxin A in rat lymphoid cells.
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Alterations induced in vitro by ochratoxin A in rat lymphoid cells.

机译:lymph曲霉毒素A体外诱导大鼠淋巴样细胞改变。

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Ochratoxin A (OTA) is a nephrotoxic mycotoxin produced by species of the genus Penicillium and Aspergillus that is present in food and feed as a natural contaminant. It modifies the immune function in animals and inhibits the proliferative response of lymphocytes in vitro. The toxic effect of OTA (0.5, 2, 20 microM) in lympho-proliferative response, natural killer (NK) cell activity, cytotoxic T lymphocytes (CTL) activity and macrophages' bacteriolytic capability was studied in vitro after 1 hour of treatment. The proliferative response of lymphocytes to concanavalin A and lipopolysaccharide was not affected by OTA; the cytotoxic activity of NK cells was dose-dependent decreased; the CTL activity was significantly decreased at the lowest concentration; the bacteriolytic activity of macrophages varied only slightly. These in vitro results reproduced, at least in part, some effects detected previously in vivo. The protein synthesis inhibition and the oxidative metabolism of OTA coupled to the prostaglandin synthesis are probably implicated in NK cells' toxicity, because the effects were reverted by the addition of phenylalanine or piroxicam to the culture medium. The induction of apoptosis seems to be the principal mechanism of action in the CTL effect. The intracellular concentration of OTA after 1 hour was analysed by HPLC and was found to be proportional to the quantity of OTA added to the culture medium for the three cell types; the presence of phenylalanine and piroxicam on the culture medium did not change the intracellular OTA concentration.
机译:ch曲霉毒素A(OTA)是一种由青霉菌和曲霉属物种产生的肾毒性霉菌毒素,它以天然污染物形式存在于食品和饲料中。它可以改变动物的免疫功能,并在体外抑制淋巴细胞的增殖反应。治疗1小时后,在体外研究了OTA(0.5、2、20 microM)对淋巴增殖反应,自然杀伤(NK)细胞活性,细胞毒性T淋巴细胞(CTL)活性和巨噬细胞溶菌能力的毒性作用。淋巴细胞对伴刀豆球蛋白A和脂多糖的增殖反应不受OTA的影响。 NK细胞的细胞毒活性呈剂量依赖性降低。在最低浓度下,CTL活性显着降低;巨噬细胞的细菌分解活性仅略有变化。这些体外结果至少部分地再现了先前在体内检测到的一些效果。蛋白质的合成抑制和OTA的氧化代谢与前列腺素的合成有关,可能与NK细胞的毒性有关,因为通过向培养基中添加苯丙氨酸或吡罗昔康可以恢复这种作用。凋亡的诱导似乎是CTL作用的主要作用机理。 1小时后,通过HPLC分析OTA的细胞内浓度,发现与三种细胞类型中添加到培养基中的OTA的量成比例。培养基中苯丙氨酸和吡罗昔康的存在不会改变细胞内OTA浓度。

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