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Cited by 43Chemotherapy-induced organ toxicity mitigationAcute Kidney Injury ResearchCircadian rhythm and melatonin

Melatonin ameliorates the drug induced nephrotoxicity: Molecular insights

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Raza, Zohaib, Naureen, Zainab·2020·Nefrología
DOI 10.1016/j.nefro.2019.06.009
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Abstract

Drug-induced nephrotoxicity is a frequent adverse event that can lead to acute or chronic kidney disease and increase the healthcare expenditure. It has high morbidity and mortality incidence in 40–70% of renal injuries and accounts for 66% cases of renal failure in elderly population. Amelioration of drug-induced nephrotoxicity has been long soughed to improve the effectiveness of therapeutic drugs. This study was conducted to review the melatonin potential to prevent the pathogenesis of nephrotoxicity induced by important nephrotoxic drugs. We analyzed the relevant studies indexed in Pubmed, Medline, Scielo and Web of science to explain the molecular improvements following melatonin co-administration with special attention to oxidative stress, inflammation and apoptosis as key players of drug-induced nephrotoxicity. A robust consensus among researchers of these studies suggested that melatonin efficiently eradicate the chain reaction of free radical production and induced the endogenous antioxidant enzymes which attenuate the lipid peroxidation of cellular membranes and subcellular oxidative stress in drug-induced nephrotoxicity. This agreement was further supported by the melatonin role in disintegration of inflammatory process through inhibition of principle pro-inflammatory or apoptotic cytokines such as TNF-α and NF-κB. These studies highlighted that alleviation of drug-induced renal toxicity is a function of melatonin potential to down regulate the cellular inflammatory and oxidative injury process and to stimulate the cellular repair or defensive mechanisms. The comprehensive nephroprotection and safer profile suggests the melatonin to be a useful adjunct to improve the safety of nephrotoxic drugs. La nefrotoxicidad inducida por medicamentos es un acontecimiento adverso frecuente que puede conducir a una nefropatía aguda o crónica, e incrementar los costes sanitarios. Presenta una incidencia elevada de morbimortalidad en el 40-70% de las lesiones renales y es responsable del 66% de los casos de insuficiencia renal entre la población de edad avanzada. La mejora de la nefrotoxicidad inducida por medicamentos es un objetivo anhelado desde hace mucho tiempo, para mejorar la eficacia de los fármacos terapéuticos. Este estudio se llevó a cabo con el propósito de revisar el potencial de la melatonina para prevenir la patogenia de la nefrotoxicidad inducida por medicamentos nefrotóxicos importantes. Analizamos los estudios relevantes indexados en Pubmed, Medline, Scielo y Web of Science, para explicar las mejoras moleculares posteriores a la administración concomitante de melatonina; prestando especial atención al estrés oxidativo, la inflamación y la apoptosis como actores fundamentales de la nefrotoxicidad inducida por medicamentos. Un sólido consenso entre los investigadores de estos estudios sugirió que la melatonina erradica de forma eficiente la reacción en cadena de producción de radicales libres e induce las enzimas antioxidantes endógenas que atenúan la peroxidación lipídica de las membranas celulares y el estrés oxidativo subcelular en la nefrotoxicidad inducida por medicamentos. Este consenso se vio respaldado por el papel de la melatonina en la desintegración del proceso inflamatorio a través de la inhibición de las principales citocinas proinflamatorias o apoptóticas, como el TNF-α y el NF-κB. Estos estudios subrayan que la mitigación de la nefrotoxicidad inducida por medicamentos se deriva del potencial de la melatonina para regular a la baja el proceso celular de lesión inflamatoria y oxidativa, y estimular la reparación celular o los mecanismos defensivos de las células. La nefroprotección exhaustiva y el perfil de seguridad más favorable sugieren que la melatonina es un complemento útil para mejorar la seguridad de los fármacos nefrotóxicos.

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Research works printed but not linked: 2

  1. Pablos MI, Guerrero JM, Ortiz GG, Agapito MT, Reiter RJ. Both melatonin and a putative nuclear melatonin receptor agonist CGP 52608 stimulate glutathione peroxidase and glutathione reductase activities in mouse brain in vivo. Neuroendocrinol Lett. 1998;18:49-58.
  2. Springate JE. Ifosfamide metabolite chloroacetaldehyde causes renal dysfunction in vivo. J Appl Toxicol. 1997;17:75-9.

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Authors
Raza, Z., & Naureen, Z.
Affiliations
  • Government College University, Faisalabad (PK)
  • Riphah International University (PK)
Corresponding author
Raza, Zohaib
ORCID
Raza, Zohaib
Venue
Nefrología
Publisher
Elsevier BV
Published
2020-01
Volume
40
Issue
1
Pages
12-25
ISSN
0211-6995 (ISSN-L)
DOI
10.1016/j.nefro.2019.06.009
OpenAlex
W2982717226
Cited by
43
References
148
Citations by year
2026: 5 · 2025: 7 · 2024: 9 · 2023: 4 · 2022: 9 · 2021: 6 · 2020: 3
FWCI
0.67
Type
journal article
Language
en
Open access
Licence
Locations
  • Nefrología (publishedVersion, cc-by-nc-nd)
  • Nefrología (English Edition) (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Chemotherapy-induced organ toxicity mitigation
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Keywords
melatonin, drug-induced nephrotoxicity, renal protection, oxidative stress, inflammation, apoptosis, lipid peroxidation, antioxidant enzymes, TNF-α, NF-κB, free radicals, kidney injury, acute kidney injury, chronic kidney disease, renal failure, elderly patients, anti-inflammatory activity
MeSH terms
Acetaminophen, Anti-Bacterial Agents, Antineoplastic Agents, Antioxidants, Chronic Disease, Free Radicals, Humans, Immunosuppressive Agents, Kidney, Kidney Diseases, Melatonin, Mitochondria, Tumor Necrosis Factor-alpha, NF-kappa B, Apoptosis, Oxidative Stress

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