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26例磷化铝中毒患者的细胞色素c氧化酶抑制情况

Cytochrome-c oxidase inhibition in 26 aluminum phosphide poisoned patients.

作者信息

Singh Surjit, Bhalla Ashish, Verma Suresh K, Kaur Amarpreet, Gill Kirandip

机构信息

Dept of Medicine, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

出版信息

Clin Toxicol (Phila). 2006;44(2):155-8. doi: 10.1080/15563650500514467.

Abstract

INTRODUCTION

Aluminum phosphide (ALP) is used worldwide to fumigate grain. ALP poisoning, though reported from different parts of world, is most common in north, northwest and central India. In the presence of moisture, ALP liberates phosphine, which is highly toxic. The mechanism of action of phosphine is not known though experimental studies show that it inhibits cytochrome-c oxidase leading to inhibition of mitochondrial oxidative phosphorylation.

PATIENTS AND METHODS

We estimated cytochrome-c oxidase activity in platelets of patients who had ingested ALP and compared them with those in healthy controls and in patients with shock due to other causes (cardiogenic shock, septic shock and hemorrhagic shock).

RESULTS

After analysis of variance using Kruskal-Wallis test followed by Mann Whitney U test, significant inhibition of cytochrome-c oxidase activity could be found in ALP-poisoned patients compared to healthy controls (z = -5.513, p < 0.001) and in patients with shock due to other causes (z = -2.344; p < 0.05). There was no significant difference in inhibition in those who survived ALP poisoning compared to those who died from ALP poisoning (t = 0.02768; p > 0.05).

CONCLUSION

Though inhibition of cytochrome-c oxidase in platelets does not have prognostic value, it suggests that interruption of mitochondrial oxidative phosphorylation as a result of cytochrome-c oxidase inhibition may lead to multi-organ dysfunction and therapeutic strategies to maintain enzyme activity may help in managing these patients.

摘要

引言

磷化铝(ALP)在全球范围内用于谷物熏蒸。尽管世界各地都有磷化铝中毒的报告,但在印度北部、西北部和中部最为常见。在有水分的情况下,磷化铝会释放出剧毒的磷化氢。尽管实验研究表明磷化氢会抑制细胞色素c氧化酶,导致线粒体氧化磷酸化受到抑制,但其作用机制尚不清楚。

患者与方法

我们估算了摄入磷化铝患者血小板中的细胞色素c氧化酶活性,并将其与健康对照组以及因其他原因导致休克的患者(心源性休克、感染性休克和失血性休克)进行比较。

结果

在使用Kruskal-Wallis检验进行方差分析,随后进行Mann-Whitney U检验后发现,与健康对照组相比,磷化铝中毒患者的细胞色素c氧化酶活性受到显著抑制(z = -5.513,p < 0.001),与因其他原因导致休克的患者相比也受到显著抑制(z = -2.344;p < 0.05)。与死于磷化铝中毒的患者相比,存活的磷化铝中毒患者在酶活性抑制方面没有显著差异(t = 0.02768;p > 0.05)。

结论

尽管血小板中细胞色素c氧化酶的抑制没有预后价值,但这表明细胞色素c氧化酶抑制导致的线粒体氧化磷酸化中断可能会导致多器官功能障碍,维持酶活性的治疗策略可能有助于治疗这些患者。

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