TY - JOUR
T1 - Mitochondrial oxidative damage by co-exposure to bisphenol A and acetaminophen in rat testes and its amelioration by melatonin
AU - Rashid, Hina
AU - Akhter, Mohammad Suhail
AU - Alshahrani, Saeed
AU - Qadri, Marwa
AU - Nomier, Yousra
AU - Sageer, Maryam
AU - Khan, Andleeb
AU - Alam, Mohammad F.
AU - Anwer, Tarique
AU - Ayoub, Razan
AU - Bahkali, Rana J.H.
N1 - Publisher Copyright:
© 2023 THE KOREAN SOCIETY FOR REPRODUCTIVE MEDICINE
PY - 2023/3/1
Y1 - 2023/3/1
N2 - Objective: Human exposure to multiple xenobiotics, over various developmental windows, results in adverse health effects arising from these concomitant exposures. Humans are widely exposed to bisphenol A, and acetaminophen is the most commonly used over-the-counter drug worldwide. Bisphenol A is a well-recognized male reproductive toxicant, and increasing evidence suggests that acetaminophen is also detrimental to the male reproductive system. The recent recognition of male reproductive system dysfunction in conditions of suboptimal reproductive outcomes makes it crucial to investigate the contributions of toxicant exposures to infertility and sub-fertility. We aimed to identify toxicity in the male reproductive system at the mitochondrial level in response to co-exposure to bisphenol A and acetaminophen, and we investigated whether melatonin ameliorated this toxicity. Methods: Male Wistar rats were divided into six groups (n=10 each): a control group and groups that received melatonin, bisphenol A, acetaminophen, bisphenol A and acetaminophen, and bisphenol A and acetaminophen with melatonin treatment. Results: Significantly higher lipid peroxidation was observed in the testicular mitochondria and sperm in the treatment groups than in the control group. Levels of glutathione and the activities of catalase, glutathione peroxidase, glutathione reductase, and manganese superoxide dismutase decreased significantly in response to the toxicant treatments. Likewise, the toxicant treatments significantly decreased the sperm count and motility, while significantly increasing sperm mortality. Melatonin mitigated the adverse effects of bisphenol A and acetaminophen. Conclusion: Co-exposure to bisphenol A and acetaminophen elevated oxidative stress in the testicular mitochondria, and this effect was alleviated by melatonin
AB - Objective: Human exposure to multiple xenobiotics, over various developmental windows, results in adverse health effects arising from these concomitant exposures. Humans are widely exposed to bisphenol A, and acetaminophen is the most commonly used over-the-counter drug worldwide. Bisphenol A is a well-recognized male reproductive toxicant, and increasing evidence suggests that acetaminophen is also detrimental to the male reproductive system. The recent recognition of male reproductive system dysfunction in conditions of suboptimal reproductive outcomes makes it crucial to investigate the contributions of toxicant exposures to infertility and sub-fertility. We aimed to identify toxicity in the male reproductive system at the mitochondrial level in response to co-exposure to bisphenol A and acetaminophen, and we investigated whether melatonin ameliorated this toxicity. Methods: Male Wistar rats were divided into six groups (n=10 each): a control group and groups that received melatonin, bisphenol A, acetaminophen, bisphenol A and acetaminophen, and bisphenol A and acetaminophen with melatonin treatment. Results: Significantly higher lipid peroxidation was observed in the testicular mitochondria and sperm in the treatment groups than in the control group. Levels of glutathione and the activities of catalase, glutathione peroxidase, glutathione reductase, and manganese superoxide dismutase decreased significantly in response to the toxicant treatments. Likewise, the toxicant treatments significantly decreased the sperm count and motility, while significantly increasing sperm mortality. Melatonin mitigated the adverse effects of bisphenol A and acetaminophen. Conclusion: Co-exposure to bisphenol A and acetaminophen elevated oxidative stress in the testicular mitochondria, and this effect was alleviated by melatonin
KW - Acetaminophen
KW - Bisphenol A
KW - Mitochondria
KW - Oxidative stress
KW - Spermatozoa
KW - Testis
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UR - http://www.scopus.com/inward/citedby.url?scp=85150785454&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/7a3cd238-d11f-3cd7-a693-ec5165ca6148/
U2 - 10.5653/cerm.2022.05568
DO - 10.5653/cerm.2022.05568
M3 - Article
C2 - 36935409
AN - SCOPUS:85150785454
SN - 2233-8233
VL - 50
SP - 26
EP - 33
JO - Clinical and Experimental Reproductive Medicine
JF - Clinical and Experimental Reproductive Medicine
IS - 1
ER -