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首页> 外文期刊>Journal of applied toxicology >Influence of paraoxon (POX) and parathion (PAT) on apoptosis: a possible mechanism for toxicity in low-dose exposure.
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Influence of paraoxon (POX) and parathion (PAT) on apoptosis: a possible mechanism for toxicity in low-dose exposure.

机译:对氧磷(POX)和对硫磷(PAT)对细胞凋亡的影响:低剂量暴露下毒性的可能机制。

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摘要

The acute effects of poisoning with organophosphorus compounds (OPCs) are well known and have been described extensively. Most of the clinical symptoms are due to inhibition of acetylcholinesterase. Although acute OPC poisoning is a well-established clinical entity, the existence of chronic poisoning due to exposure to low levels of OPC (below the threshold required for cholinergic clinical symptoms) is a hotly debated issue. Recent studies have suggested the involvement of OPCs in apoptotic processes. However, the mechanisms by which they modulate this process are poorly investigated. In the present study we evaluated the toxic effect of different concentrations of paraoxon (POX) and parathion (PAT) in murine EL4 T lymphocytes. We examined cellular responses, including induction of apoptosis, involvement of a caspase cascade, the activity of effector caspase (caspase-3) and the biochemical and morphological changes that are the hallmarks of classical apoptosis. The results of our study indicate that at doses below IC(50) POX is a potent inducer of apoptosis, as opposed to PAT that shows little apoptotic effect.
机译:有机磷化合物(OPC)中毒的急性影响是众所周知的,并已得到广泛描述。大多数临床症状是由于抑制乙酰胆碱酯酶引起的。尽管急性OPC中毒是公认的临床实体,但是由于暴露于低水平的OPC(低于胆碱能临床症状所需的阈值)而导致的慢性中毒的存在是一个备受争议的问题。最近的研究表明,OPCs参与凋亡过程。但是,他们调制此过程的机制研究很少。在本研究中,我们评估了不同浓度的对氧磷(POX)和对硫磷(PAT)在鼠EL4 T淋巴细胞中的毒性作用。我们检查了细胞应答,包括细胞凋亡的诱导,caspase级联的参与,效应子caspase(caspase-3)的活性以及经典化学凋亡的生化和形态变化。我们的研究结果表明,在低于IC(50)的剂量下,POX是有效的凋亡诱导剂,而PAT则几乎没有凋亡作用。

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