Emerging contaminant triclosan incites endocrine disruption, reproductive impairments and oxidative stress in the commercially important carp, Catla (Labeo catla): An insight through molecular, histopathological and bioinformatic approach.

Autor: Adhikari A; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India., Das BK; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India. Electronic address: basantakumard@gmail.com., Ganguly S; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India., Nag SK; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India., Sadhukhan D; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India., Raut SS; ICAR- Central Inland Fisheries Research Institute, Barrackpore, Kolkata 700120, India.
Jazyk: angličtina
Zdroj: Comparative biochemistry and physiology. Toxicology & pharmacology : CBP [Comp Biochem Physiol C Toxicol Pharmacol] 2023 Jun; Vol. 268, pp. 109605. Date of Electronic Publication: 2023 Mar 10.
DOI: 10.1016/j.cbpc.2023.109605
Abstrakt: Triclosan (TCS), a broad-spectrum antimicrobial agent is ubiquitous in aquatic ecosystems; however, the mechanisms regarding TCS-induced reproductive toxicity in the teleost still remains uncertain. In this context, Labeo catla were subjected to sub-lethal doses of TCS for 30 days and variations in expression of genes and hormones comprising the hypothalamic-pituitary-gonadal (HPG) axis along with alterations in sex steroids were evaluated. Moreover, manifestation of oxidative stress, histopathological alterations, in silico docking and the potential to bioaccumulate were also investigated. Exposure to TCS may lead to an inevitable onset of the steroidogenic pathway through its interaction at several loci along the reproductive axis: TCS stimulated synthesis of kisspeptin 2 (Kiss 2) mRNAs which in turn prompts the hypothalamus to secrete gonadotropin-releasing hormone (GnRH), resulting in elevated serum 17β-estradiol (E 2 ) as a consequence; TCS exposure increased aromatase synthesis by brain, which by converting androgens to oestrogens may raise E 2 levels; Moreover, TCS treatment resulted in elevated production of GnRH and gonadotropins by the hypothalamus and pituitary, respectively resulting in the induction of E 2 . The elevation in serum E 2 may be linked to abnormally elevated levels of vitellogenin (Vtg) with harmful consequences evident as hypertrophy of hepatocytes and increment in hepatosomatic indices. Additionally, molecular docking studies revealed potential interactions with multiple targets viz. Vtg and luteinizing hormone (LH). Furthermore, TCS exposure induced oxidative stress and caused extensive damage to tissue architecture. This study elucidated molecular mechanisms underlying TCS-induced reproductive toxicity and the need for regulated use and efficient alternatives which could suffice for TCS.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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