Acetate Abates Arsenic-Induced Male Reproductive Toxicity by Suppressing HDAC and Uric Acid-Driven Oxido-inflammatory NFkB/iNOS/NO Response in Rats.

Autor: Besong EE; Department of Physiology, Faculty of Basic Medical Sciences, Ebonyi State University, Abakaliki, Nigeria., Akhigbe TM; Breeding and Plant Genetics Unit, Department of Agronomy, Osun State University, Osogbo, Osun State, Nigeria.; Reproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria., Obimma JN; Department of Physiology, Faculty of Basic Medical Sciences, Ebonyi State University, Abakaliki, Nigeria., Obembe OO; Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria., Akhigbe RE; Reproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria. akhigberoland@gmail.com.; Department of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria. akhigberoland@gmail.com.
Jazyk: angličtina
Zdroj: Biological trace element research [Biol Trace Elem Res] 2024 Jun; Vol. 202 (6), pp. 2672-2687. Date of Electronic Publication: 2023 Sep 19.
DOI: 10.1007/s12011-023-03860-4
Abstrakt: Arsenic is associated with male reproductive toxicity through histone deacetylation and oxido-inflammatory injury. Notwithstanding, short-chain fatty acids such as acetate exert anti-oxido-inflammatory activities and inhibit histone deacetylation. This study investigated the impact of acetate on arsenic-induced male reproductive toxicity. Forty eight adult male Wistar rats were allotted into any of these four groups (n = 12 rats per group): vehicle-treated, sodium acetate-treated, arsenic-exposed, and arsenic-exposed + sodium acetate-treated. The results revealed that arsenic exposure prolonged the latencies of mount, intromission, and ejaculation and reduced the frequencies of mount, intromission, and ejaculation, as well as mating and fertility indices, litter size and weight, anogenital distance, anogenital index, and survival rate in male F1 offspring at weaning. Also, arsenic reduced the circulating levels of gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone, and testosterone and testicular 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase activities. In addition, arsenic reduced the daily and total spermatid production, sperm count, motility, and viability but increased the percentage of sperm cells with abnormal morphology. Furthermore, arsenic increased testicular xanthine oxidase activity, uric acid, and malondialdehyde levels, and reduced glutathione content, superoxide dismutase and catalase activities, total antioxidant capacity, and Nrf2 level. More so, arsenic exposure increased testicular iNOS activity and nitric oxide (NO), TNF-α, IL-1β, IL-6, and NFkB levels as well as Bax, caspase 9, and caspase 3 activities, and reduced Bcl-2. These findings were associated with arsenic-induced increase in testicular arsenic concentration, histone deacetylase activity, and reduced testicular weight. Histopathological examination revealed that arsenic also disrupted testicular histoarchitecture, which was accompanied by altered testicular planimetry and reduced spermatogenic cells. Notwithstanding, sodium acetate alleviated arsenic-induced sexual dysfunction as well as biochemical and histological alterations. These were accompanied acetate-driven downregulation of histone deacetylase (HDAC) activity. Succinctly, acetate attenuated arsenic-induced male reproductive toxicity by suppressing HDAC and uric acid-driven oxido-inflammatory NFkB/iNOS/NO response.
(© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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