Chemosphere · 2023
Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Ogunsuyi Opeoluwa M, Fasakin Peter T, Ajibiye Oluwatobi P, Ogunsuyi Olusegun I, Adekoya Khalid O
Аннотация
Perfluoroundecanoic acid (PFUnA) is an eleven carbon-chain compound that belongs to the perfluoroalkyl carboxylic acid family. It has been detected in the human blood, effluents, and surface/ground waters, but its toxic effects to the DNA and reproductive system remain unclear. This study was aimed at exploring the toxicity of PFUnA on the hepatic DNA, organ-system and reproductive system in orally treated male Swiss mice. In this present study, administration of PFUnA for 28 days with five doses (0.1, 0.3, 05, 0.7 and 1.0 mg kg-1 b.w./d) in male Swiss mice induced significant hepatic DNA damage which was observed using the alkaline comet assay and equally altered hematological and clinical biochemical parameters. In addition to testicular atrophy, sperm count and sperm motility significantly decreased while sperm abnormalities increased after 35 days exposure. Serum LH and FSH levels were remarkably increased while serum testosterone levels were strikingly reduced. Histopathology revealed the liver, kidney, and testis as potential targets of PFUnA toxicity. Increased activities of superoxide dismutase (SOD) and catalase (CAT), as well as levels of glutathione-s-transferase (GST) and reduced glutathione (GSH), with consistent reduction of glutathione peroxidase (GPx) and reduced glutathione (GSH) in the liver and testis induced oxidative stress. In conclusion, PFUnA exhibited both genotoxicity and reproductive toxicity via oxidative stress induction.