Bisphenol S induced dysregulations in liver; iron regulatory genes and inflammatory mediators in male Wistar rats

Ghafoor, Shazia; Abbasi, Muddasir Hassan; Khawar, Muhammad Babar; Tayyeb, Asima; Saleem, Tayyaba; Ashfaq, Isbah; Sheikh, Nadeem

doi:10.1007/s11356-022-21672-2

Cited by 5 publications

(6 citation statements)

References 44 publications

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“…In addition, animals of the VitE + BPS-D group showed a significant increase compared with those in the other experimental groups in BUN, total cholesterol, ALT, and urea. The increase in hepatic enzymes observed in the present article was like that in other studies evaluating BPS' effect in Wistar rats [81], where the authors considered that BPS produced potential hepatic intoxication [81]. In addition, the effects caused by BPS on the liver function observed in the present research were similar to those caused by BPA [84,85].…”

Section: Discussionsupporting

confidence: 86%

Vitamin E (α-Tocopherol) Does Not Ameliorate the Toxic Effect of Bisphenol S on the Metabolic Analytes and Pancreas Histoarchitecture of Diabetic Rats

Peña-Corona,

Vargas-Estrada,

Chávez-Corona

et al. 2023

Toxics

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This study investigated whether the coadministration of vitamin E (VitE) diminishes the harmful effects provoked by plasticizer bisphenol S (BPS) in the serum metabolites related to hepatic and renal metabolism, as well as the endocrine pancreatic function in diabetic male Wistar rats. Rats were divided into five groups (n = 5–6); the first group was healthy rats (Ctrl group). The other four groups were diabetic rats induced with 45 mg/kg bw of streptozotocin: Ctrl-D (diabetic control); VitE-D (100 mg/kg bw/d of VitE); BPS-D (100 mg/kg bw/d of BPS); The animals from the VitE + BPS-D group were administered 100 mg/kg bw/d of VitE + 100 mg/kg bw/d of BPS. All compounds were administered orally for 30 days. Body weight, biochemical assays, urinalysis, glucose tolerance test, pancreas histopathology, proximate chemical analysis in feces, and the activity of antioxidants in rat serum were assessed. The coadministration of VitE + BPS produced weight losses, increases in 14 serum analytes, and degeneration in the pancreas. Therefore, the VitE + BPS coadministration did not have a protective effect versus the harmful impact of BPS or the diabetic metabolic state; on the contrary, it partially aggravated the damage produced by the BPS. VitE is likely to have an additive effect on the toxicity of BPS.

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Section: Discussionsupporting

confidence: 86%

Vitamin E (α-Tocopherol) Does Not Ameliorate the Toxic Effect of Bisphenol S on the Metabolic Analytes and Pancreas Histoarchitecture of Diabetic Rats

Peña-Corona,

Vargas-Estrada,

Chávez-Corona

et al. 2023

Toxics

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“…23,38 The dose and timing of administration of BPS and melatonin were selected based on previous reports. 7,23,[38][39][40][41]…”

Section: Methodsmentioning

confidence: 99%

“…Melatonin treatment was started 24 h preceding BPS administration 23,38 . The dose and timing of administration of BPS and melatonin were selected based on previous reports 7,23,38–41 …”

Section: Methodsmentioning

confidence: 99%

“…6 BPS induces oxidative stress in liver, kidney, brain, and germ cells. [7][8][9] BPS is known to impair human granulosa and theca cell steroidogenesis in-vitro, while in-vivo reports regarding BPS-induced ovarian dysfunction are scanty. Previous studies suggest that oxidative stress increased caspase-3 expression leading to granulosa cell (GC) apoptosis.…”

Section: Introductionmentioning

confidence: 99%

“…Normal ovarian functions such as oocyte maturation, ovulation, and luteinization involve interactions between inflammatory and oxidative stress responses but their continuous existence induces generation of reactive oxygen species (ROS) disrupting the redox homeostasis within ovary 6 . BPS induces oxidative stress in liver, kidney, brain, and germ cells 7–9 . BPS is known to impair human granulosa and theca cell steroidogenesis in‐vitro, while in‐vivo reports regarding BPS‐induced ovarian dysfunction are scanty.…”

Section: Introductionmentioning

confidence: 99%

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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

Pal

Sahu

Verma

et al. 2023

Journal of Pineal Research

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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.

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Mitochondrial Lipid Peroxidation and Microsomal Drug-metabolizing Enzyme Activity of Rat Hepatotoxicity under Heavy Metals from Slag Waste Exposure

Wan²,

Kuang

et al. 2023

Cell Biochem Biophys

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Heavy metals from slag waste (HMSWs) have been a long-term concern around the world, posing serious environmental and visceral toxicity, especially hepatotoxicity. Investigating the leaching behavior and hepatotoxicity of HMSWs is of great signi cance. Based on the toxicogenomic analysis, the targets and related signaling pathways of heavy metal-induced liver injury were predicted, and the effects of different HMSWs on mitochondrial lipid peroxidation injury and microsomal drug-metabolizing enzyme activities in rats were experimentally explored. The results showed that different heavy metals might have the function of interfering with physiological processes such as oxidative stress, cell death, and energy metabolism regulation in vivo, and participate in the regulation of HIF-1 signaling pathway, peroxisomes, drug metabolism-cytochrome P450, ferroptosis, and other signaling pathways. HMSWs exposure caused weight loss, and signi cantly increased lactate dehydrogenase (LDH), malondialdehyde (MDA), alanine transaminase (ALT), and aspartate transaminase (AST) in different groups of rat liver, suggesting the presence of mitochondrial lipid peroxidation damage. Meanwhile, the activities of superoxide dismutase (SOD) and mitochondrial membrane potential (MMP) in the liver were signi cantly decreased, and microsomal Cytochrome P450 1A2 (CYP1A2) and 3A1 (CYP3A1) enzyme activities were induced, predicting the involvement of the microsomal drug-metabolizing enzymes. These results indicated that metabolic interplay between microsomes and other subcellular organelles including mitochondria and peroxisome could be involved in heavy metals-induced liver injury.

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Bisphenol S induced dysregulations in liver; iron regulatory genes and inflammatory mediators in male Wistar rats

Cited by 5 publications

References 44 publications

Vitamin E (α-Tocopherol) Does Not Ameliorate the Toxic Effect of Bisphenol S on the Metabolic Analytes and Pancreas Histoarchitecture of Diabetic Rats

Vitamin E (α-Tocopherol) Does Not Ameliorate the Toxic Effect of Bisphenol S on the Metabolic Analytes and Pancreas Histoarchitecture of Diabetic Rats

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

Mitochondrial Lipid Peroxidation and Microsomal Drug-metabolizing Enzyme Activity of Rat Hepatotoxicity under Heavy Metals from Slag Waste Exposure

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