@article{ref1,
title="Pathological changes induced by phosphine poisoning: a study on 8 children",
journal="International journal of legal medicine",
year="2019",
author="Liang, Yue and Tong, Fang and Huang, Fang and Liu, Yuluo and Zhu, Longlong and Le Grange, Jehane Michael and He, Guanglong and Zhou, Yiwu",
volume="ePub",
number="ePub",
pages="ePub-ePub",
abstract="Aluminum phosphide (ALP) has been extensively used as an economical and effective insecticide, rodenticide, and fumigant. The active ingredient of ALP is phosphine (PH<sub>3</sub>), the use of which can lead to accidental inhalation and mass poisoning with high mortality. Exposure to PH<sub>3</sub> will give rise to global damage in the human body. This study reviewed 4 fatal accidents including 8 children with PH<sub>3</sub> poisoning and aimed to determine the pathological changes that resulted from exposure to PH<sub>3</sub> and, secondly, aimed to determine whether oxidative stress was involved in PH<sub>3</sub>-induced neurotoxicity using histopathological and immunohistochemistry (IHC) methods. After focusing on the pathological changes on the major organs, we found severe damage induced by PH<sub>3</sub> in many systems, especially the neurological system, including neuronal, axonal, and vascular injuries as well as oxidative damage with increased expression of 4-hydroxy-2-trans-nonenal (4HNE), 8-hydroxy-2'-deoxyguanosine (8-OH-dG), and 3-nitrotyrosine (3-NT) in the brain, which indicated that oxidative stress was a crucial mechanism for neuronal death in PH<sub>3</sub> toxicity. Moreover, we observed severe myocardial and hepatocellular fatty degeneration in the tissues of the heart and liver. We considered that these characteristic changes are a suggestive sign of PH<sub>3</sub> poisoning and partly explained the toxic mechanism of PH<sub>3</sub> (inhibition of mitochondrial oxidative phosphorylation). We hope that this research could improve the understanding of the toxicity of PH<sub>3</sub> in both forensic and clinical practice.<p /> <p>Language: en</p>",
language="en",
issn="0937-9827",
doi="10.1007/s00414-019-02169-z",
url="http://dx.doi.org/10.1007/s00414-019-02169-z"
}