Melatonin Rescues Renal Mitochondria From Multiple Stressors–Induced Oxidative Stress

ABSTRACT The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisp...

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Published inBasic & clinical pharmacology & toxicology Vol. 136; no. 5; pp. e70031 - n/a
Main Authors Alshahrani, Saeed, Sultan, Muhammad H., Rashid, Hina, Alam, Firoz, Khan, Andleeb, Akhter, Mohammad Suhail, Qamri, Derayat, Beigh, Saba, Riyaz, Farhana
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.05.2025
Subjects
Acetaminophen
Acetaminophen - toxicity
Analgesics
Animals
Antioxidants
Antioxidants - pharmacology
Benzhydryl Compounds - toxicity
Biomarkers - blood
Bisphenol A
Bisphenol A Compounds
Creatinine
Epinephrine
Hydrogen peroxide
Inflammation
Interleukin 6
kidney
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Male
Melatonin
Melatonin - pharmacology
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Oxidation
Oxidative stress
Oxidative Stress - drug effects
Phenols - toxicity
Proteins
Rats
Rats, Wistar
Renal function
Superoxide dismutase
Toxins
Tumor necrosis factor-α
Uric acid
Xenobiotics
kidney
acetaminophen
bisphenol A
inflammation
mitochondria
oxidative stress
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Abstract ABSTRACT The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85‐μmol H2O2/min/mg protein, GPx: 189.57‐nmol NADPH/min/mg protein, GR: 96.62‐nmol NADPH/min/mg protein, MnSOD: 107.24‐nmol (−) epinephrine/min/mg protein, IL‐6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74‐μmol H2O2/min/mg protein, GPx: 422.74‐nmol NADPH/min/mg protein, GR: 136.91‐nmol NADPH/min/mg protein, MnSOD: nmol (−) epinephrine prevented from oxidation/min/mg protein, IL‐6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen‐induced renal damage by enhancing antioxidant defences and reducing inflammation.
AbstractList The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85‐μmol H 2 O 2 /min/mg protein, GPx: 189.57‐nmol NADPH/min/mg protein, GR: 96.62‐nmol NADPH/min/mg protein, MnSOD: 107.24‐nmol (−) epinephrine/min/mg protein, IL‐6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74‐μmol H 2 O 2 /min/mg protein, GPx: 422.74‐nmol NADPH/min/mg protein, GR: 136.91‐nmol NADPH/min/mg protein, MnSOD: nmol (−) epinephrine prevented from oxidation/min/mg protein, IL‐6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen‐induced renal damage by enhancing antioxidant defences and reducing inflammation.
The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85-μmol H2O2/min/mg protein, GPx: 189.57-nmol NADPH/min/mg protein, GR: 96.62-nmol NADPH/min/mg protein, MnSOD: 107.24-nmol (-) epinephrine/min/mg protein, IL-6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74-μmol H2O2/min/mg protein, GPx: 422.74-nmol NADPH/min/mg protein, GR: 136.91-nmol NADPH/min/mg protein, MnSOD: nmol (-) epinephrine prevented from oxidation/min/mg protein, IL-6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen-induced renal damage by enhancing antioxidant defences and reducing inflammation.The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85-μmol H2O2/min/mg protein, GPx: 189.57-nmol NADPH/min/mg protein, GR: 96.62-nmol NADPH/min/mg protein, MnSOD: 107.24-nmol (-) epinephrine/min/mg protein, IL-6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74-μmol H2O2/min/mg protein, GPx: 422.74-nmol NADPH/min/mg protein, GR: 136.91-nmol NADPH/min/mg protein, MnSOD: nmol (-) epinephrine prevented from oxidation/min/mg protein, IL-6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen-induced renal damage by enhancing antioxidant defences and reducing inflammation.
The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85‐μmol H2O2/min/mg protein, GPx: 189.57‐nmol NADPH/min/mg protein, GR: 96.62‐nmol NADPH/min/mg protein, MnSOD: 107.24‐nmol (−) epinephrine/min/mg protein, IL‐6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74‐μmol H2O2/min/mg protein, GPx: 422.74‐nmol NADPH/min/mg protein, GR: 136.91‐nmol NADPH/min/mg protein, MnSOD: nmol (−) epinephrine prevented from oxidation/min/mg protein, IL‐6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen‐induced renal damage by enhancing antioxidant defences and reducing inflammation.
ABSTRACT The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85‐μmol H2O2/min/mg protein, GPx: 189.57‐nmol NADPH/min/mg protein, GR: 96.62‐nmol NADPH/min/mg protein, MnSOD: 107.24‐nmol (−) epinephrine/min/mg protein, IL‐6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74‐μmol H2O2/min/mg protein, GPx: 422.74‐nmol NADPH/min/mg protein, GR: 136.91‐nmol NADPH/min/mg protein, MnSOD: nmol (−) epinephrine prevented from oxidation/min/mg protein, IL‐6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen‐induced renal damage by enhancing antioxidant defences and reducing inflammation.
The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of xenobiotics in humans causes deleterious effects in the kidneys. In the present study, we observed the toxic effect of a coexposure of bisphenol A and acetaminophen on the renal function and renal mitochondria of Wistar rats and its amelioration by melatonin. The animals were grouped and treated for 4 weeks as follows: (I) control; (II) melatonin; (III) bisphenol A; (IV) acetaminophen; (V) bisphenol A and acetaminophen; and (VI) bisphenol A, acetaminophen and melatonin. Coadministration of bisphenol A and acetaminophen exposure significantly impaired renal function, elevating creatinine (2.28 mg/dL), BUN (65.42 mg/dL) and uric acid (6.11 mg/dL), while increasing oxidative stress and inflammatory markers (CAT: 3.85-μmol H O /min/mg protein, GPx: 189.57-nmol NADPH/min/mg protein, GR: 96.62-nmol NADPH/min/mg protein, MnSOD: 107.24-nmol (-) epinephrine/min/mg protein, IL-6: 1750 pg/mL, TNFα: 1677 pg/mL). Melatonin coadministration improved renal markers (creatinine: 1.60 mg/dL, BUN: 45.59 mg/dL, uric acid: 4.61 mg/dL) and partially restored antioxidant defences and inflammatory markers (CAT: 5.74-μmol H O /min/mg protein, GPx: 422.74-nmol NADPH/min/mg protein, GR: 136.91-nmol NADPH/min/mg protein, MnSOD: nmol (-) epinephrine prevented from oxidation/min/mg protein, IL-6: 1677 pg/mL, TNFα: 900 pg/mL). These findings suggest that melatonin mitigates bisphenol A and acetaminophen-induced renal damage by enhancing antioxidant defences and reducing inflammation.
Author Alshahrani, Saeed
Akhter, Mohammad Suhail
Khan, Andleeb
Riyaz, Farhana
Rashid, Hina
Beigh, Saba
Sultan, Muhammad H.
Alam, Firoz
Qamri, Derayat
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Issue 5
Keywords kidney
acetaminophen
bisphenol A
inflammation
mitochondria
oxidative stress
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License 2025 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society). Published by John Wiley & Sons Ltd.
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The authors gratefully acknowledge the funding of the Deanship of Graduate Studies and Scientific Research, Jazan University, Saudi Arabia, through Project Number: RG24‐M022.
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2024; 38
2013; 6
2006; 20
2018; 4
2019; 20
2023; 133
1951; 193
1985
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2021; 8
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2021; 269
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1982; 31
1984; 105
2020; 104
2018; 23
2019; 141
2021; 180
2017; 109
2016; 6
2021; 15
2018; 2018
2010; 48
2021; 11
2019; 42
2019; 44
2021; 17
1999; 37
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2022; 12
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2020; 27
2005; 12
2023; 50
2018; 14
2025; 82
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Snippet ABSTRACT The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array...
The renal system is a significant organ system vulnerable to stress due to its physiological function of toxin elimination. Exposure to a wide array of...
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wiley
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Publisher
StartPage e70031
SubjectTerms Acetaminophen
Acetaminophen - toxicity
Analgesics
Animals
Antioxidants
Antioxidants - pharmacology
Benzhydryl Compounds - toxicity
Biomarkers - blood
Bisphenol A
Bisphenol A Compounds
Creatinine
Epinephrine
Hydrogen peroxide
Inflammation
Interleukin 6
kidney
Kidney - drug effects
Kidney - metabolism
Kidney - pathology
Male
Melatonin
Melatonin - pharmacology
Mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Oxidation
Oxidative stress
Oxidative Stress - drug effects
Phenols - toxicity
Proteins
Rats
Rats, Wistar
Renal function
Superoxide dismutase
Toxins
Tumor necrosis factor-α
Uric acid
Xenobiotics
Title Melatonin Rescues Renal Mitochondria From Multiple Stressors–Induced Oxidative Stress
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbcpt.70031
https://www.ncbi.nlm.nih.gov/pubmed/40183215
https://www.proquest.com/docview/3194331937
https://www.proquest.com/docview/3186355867
Volume 136
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