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接触中国粉尘会加剧环磷酰胺对小鼠诱导的睾丸毒性。

Exposure to China dust exacerbates testicular toxicity induced by cyclophosphamide in mice.

作者信息

Kim Woong-Il, Lim Je-Oh, Pak So-Won, Lee Se-Jin, Shin In-Sik, Moon Changjong, Heo Jeong-Doo, Kim Jong-Choon

机构信息

College of Veterinary Medicine, Chonnam National University, 77 Yongbong-ro, Buk-gu, 61186 Gwangju, Republic of Korea.

Bioenvironmental Science & Technology Division, Korea Institute of Toxicology, 52834 Jinju, Republic of Korea.

出版信息

Toxicol Res. 2022 Sep 23;39(1):115-125. doi: 10.1007/s43188-022-00149-x. eCollection 2023 Jan.

DOI:10.1007/s43188-022-00149-x
PMID:36726831
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9839921/
Abstract

This study investigated the potential effects of China dust (CD) exposure on cyclophosphamide (CP)-induced testicular toxicity in mice, focusing on spermatogenesis and oxidative damage. CP treatment reduced testicular and epididymal weight and sperm motility and enhanced sperm abnormality. Histopathological examination presented various morphological alterations in the testis, including increased exfoliation of spermatogenic cells, degeneration of early spermatogenic cells, vacuolation of Sertoli cells, a decreased number of spermatogonia/spermatocytes/spermatids, along with a high number of apoptotic cells. In addition, the testis exhibited reduced glutathione (GSH) levels and glutathione reductase (GR) activity and enhanced malondialdehyde (MDA) concentration. Meanwhile, CD exposure exacerbated testicular histopathological alterations induced by CP. CD exposure also aggravated oxidative damage by increasing the lipid peroxidative product MDA and decreasing GSH levels and antioxidant enzyme activities in the testis. These results suggest that CD exposure exacerbates CP-induced testicular toxicity in mice, which might be attributed to the induction of lipid peroxidation and reduced antioxidant activity.

摘要

本研究调查了暴露于中国沙尘(CD)对环磷酰胺(CP)诱导的小鼠睾丸毒性的潜在影响,重点关注精子发生和氧化损伤。CP处理降低了睾丸和附睾重量以及精子活力,并增加了精子异常率。组织病理学检查显示睾丸出现各种形态学改变,包括生精细胞脱落增加、早期生精细胞变性、支持细胞空泡化、精原细胞/精母细胞/精子细胞数量减少,同时伴有大量凋亡细胞。此外,睾丸中的谷胱甘肽(GSH)水平和谷胱甘肽还原酶(GR)活性降低,丙二醛(MDA)浓度升高。同时,CD暴露加剧了CP诱导的睾丸组织病理学改变。CD暴露还通过增加脂质过氧化产物MDA以及降低睾丸中的GSH水平和抗氧化酶活性而加重氧化损伤。这些结果表明,CD暴露会加剧CP诱导的小鼠睾丸毒性,这可能归因于脂质过氧化的诱导和抗氧化活性的降低。

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