Browsing by Author "Aishwarya Sahu"

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Bisphenol S dysregulates thyroid hormone homeostasis; Testicular survival, redox and metabolic status: Ameliorative actions of melatonin
(Elsevier B.V., 2023) Aishwarya Sahu; Rakesh Verma
Bisphenol S (BPS) is an incipient threat for reproductive health augmenting societal burden of infertility worldwide. In the present study, we investigated the mechanism of BPS induced testicular dysfunctions and protective actions of melatonin in mice. BPS (150 mg/kg BW) treatment reduced serum T3/T4, testosterone and elevated insulin levels along with adverse effect on thyroid and testicular histoarchitecture. Further, BPS treatment compromised sperm quality, reduced mRNA expression of steroidogenic (StAR/CYP11A1) markers, elevated oxidative load and disrupts metabolic status. However, melatonin (5 mg/kg BW) administration to BPS treated mice showed improved hormonal/histological parameters, enhanced thyroid hormone (TR-α/Dio-2)/melatonin (MT-1) receptor expressions. Further, melatonin treatment modulated the expression of testicular survival/redox (SIRT1/PGC-1α/FOXO-1, Nrf2/HO-1, p-JAK2/p-STAT3), proliferative (PCNA) and metabolic (IR/pAKT/GLUT-1) markers. Furthermore, melatonin treatment enhanced testicular antioxidant status and reduced caspase-3 expression. In conclusion, our results showed that BPS induces endocrine/oxidative and metabolic anomalies while melatonin improved male reproductive health. © 2023 Elsevier B.V.
BPS-induced ovarian dysfunction: Protective actions of melatonin via modulation of SIRT-1/Nrf2/NFĸB and IR/PI3K/pAkt/GLUT-4 expressions in adult golden hamster
(John Wiley and Sons Inc, 2023) Sriparna Pal; Aishwarya Sahu; Rakesh Verma; Chandana Haldar
Ever-increasing occurrence of plastic-manufacturing industries leads to environmental pollution that has been associated with declined human health and increased incidence of compromised reproductive health. Female subfertility/infertility is a complex phenomenon and environmental toxicants as well as lifestyle factors have a crucial role to play. Bisphenol S (BPS) was believed to be a “safer” replacement of bisphenol A (BPA) but recent data documented its neurotoxic, hepatotoxic, nephrotoxic, and reprotoxic attributes. Hence based on the scarcity of reports, we investigated molecular insights into BPS-induced ovarian dysfunction and protective actions of melatonin against it in adult golden hamsters, Mesocricetus auratus. Hamsters were administered with melatonin (3 mg/kg BW i.p. alternate days) and BPS (150 mg/kg BW orally every day) for 28 days. BPS treatment disrupted hypothalamo–pituitary–ovarian (HPO) axis as evident by reduced gonadotropins such as luteinizing hormone (LH) and follicle-stimulating hormone (FSH), ovarian steroids such as estradiol (E2) and progesterone (P4), thyroid hormones namely triiodothyronine (T3) and thyroxine (T4) and melatonin levels along with their respective receptors (ERα, TRα, and MT-1) thereby reducing ovarian folliculogenesis. BPS exposure also led to ovarian oxidative stress/inflammation by increasing reactive oxygen species and metabolic disturbances. However, melatonin supplementation to BPS restored ovarian folliculogenesis/steroidogenesis as indicated by increased number of growing follicles/corpora lutea and E2/P4 levels. Further, melatonin also stimulated key redox/survival markers such as silent information regulator of transcript-1 (SIRT-1), forkhead box O-1 (FOXO-1), nuclear factor E2-related factor-2 (Nrf2), and phosphoinositide 3-kinase/protein kinase B (PI3K/pAkt) expressions along with enhanced ovarian antioxidant capacity. Moreover, melatonin treatment reduced inflammatory load including ovarian nuclear factor kappa-B (NFĸB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) expressions, serum tumor necrosis factor α (TNFα), C-reactive protein (CRP) and nitrite–nitrate levels as well as upregulated ovarian insulin receptor (IR), glucose uptake transporter-4 (GLUT-4), connexin-43, and proliferating cell nuclear antigen (PCNA) expressions in ovary thereby ameliorating inflammatory and metabolic alterations due to BPS. In conclusion, we found severe deleterious impact of BPS on ovary while melatonin treatment protected ovarian physiology from these detrimental changes suggesting it to be a potential preemptive candidate against environmental toxicant-compromised female reproductive health. © 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Melatonin Improves Lactational Bisphenol S Induced Pre-Pubertal and Pubertal Testicular Impairments in Offspring
(Springer Nature, 2025) Aishwarya Sahu; Vartika Malik; Rakesh Verma
Lactational period is of extreme importance for nourishing and fostering growth in neonates. Bisphenol S (BPS) a congener of bisphenol A (BPA) is an emerging environmental toxicant reported to have deleterious effects on reproductive health. Indirect exposure of BPS to the suckling infants via breastmilk is less explored although it can lead to various public health issues. Therefore, we investigated harmful effects of lactational BPS exposure on pre-pubertal and pubertal testicular functions of the offspring and its possible amelioration by melatonin. Lactating dams were divided into 4 groups: control, melatonin treated (3 mg/kg BW), BPS treated (150 mg/kg BW) and BPS + melatonin co-treatment; the male offspring were evaluated at pre-pubertal (PND 22) and pubertal (PND 42) testicular developmental stages. Lactational BPS exposure affected testicular physiology, led to histological abnormalities, hormonal imbalance, alters blood-testis-barrier (E-cadherin/connexin-43), redox modulators (SIRT-1/FOXO-1/PGC-1α; Nrf2/HO-1/pSTAT-3) and germ cell dynamicity (PCNA/TUNEL positive cells) in both pre-pubertal and pubertal mice. However, melatonin supplementation to BPS exposed lactating mothers improved testicular histoarchitecture in offspring, enhanced testicular antioxidant status, modulated expression of redox/survival and BTB markers that promoted germ cell proliferation. In conclusion, our study shows that lactational BPS exposure could be deleterious to testicular physiology that may result in male infertility/subfertility in later life while melatonin supplementation improves the reproductive health compromised by lactational BPS exposure. © The Author(s), under exclusive licence to Society for Reproductive Investigation 2025.