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The effect of melatonin on capecitabine-induced hepatic and renal toxicity in rats.
Tavakoli Pirzaman, Ali; Mansoori, Razieh; Hosseini, Seyed Mohammad; Abolhosseini, Ali; Khosravi, Sahar; Moghadamnia, Ali Akbar; Kazemi, Sohrab.
Afiliación
  • Tavakoli Pirzaman A; Student Research Committee, Babol University of Medical Science, Babol, Iran.
  • Mansoori R; Department of Pharmacology and Toxicology, School of Medicine, Babol University of Medical Science, Babol, Iran.
  • Hosseini SM; Department of Veterinary Pathology, Babol-Branch, Islamic Azad University, Babol, Iran.
  • Abolhosseini A; Student Research Committee, Babol University of Medical Science, Babol, Iran.
  • Khosravi S; Cancer Research Center, Health Research Institute, Babol University of Medical Science, Babol, Iran.
  • Moghadamnia AA; Pharmaceutical Sciences Research Center, Health Research Institute, Babol University of Medical Science, Babol, Iran.
  • Kazemi S; Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Science, Babol, Iran.
Hum Exp Toxicol ; 43: 9603271231223506, 2024.
Article en En | MEDLINE | ID: mdl-38179616
ABSTRACT

BACKGROUND:

Capecitabine (CAPE), an antimetabolite chemotherapy, can induce hepatic and renal toxicity. Melatonin (MEL), a neurohormone, possesses antioxidant, anti-apoptotic and anti-inflammatory effects. This study investigated the impact of MEL on capecitabine-induced hepatic and renal toxicity. METHODS AND MATERIALS Twenty-five male Wistar rats were categorized into five groups for the study. The groups included a control group, MEL10 group (rats receiving daily intraperitoneal injections of 5 mg/kg MEL), CAPE 500 group (rats receiving weekly intraperitoneal injections of 500 mg/kg CAPE), CAPE + MEL five group, and CAPE + MEL 10 group. All groups were treated for a duration of 6 weeks. Various hematological, serological, biochemical, and histopathological assessments were conducted to evaluate the objective of the study.

RESULTS:

The administration of CAPE led to significant liver and kidney toxicity, as evidenced by elevated levels of malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), as well as serological markers including AST, ALT, ALP, BUN, and creatinine. CAPE exposure also resulted in a reduction in total antioxidant capacity (TAC) and glutathione peroxidase (GPx) levels. Histological examination revealed hyperemia in both liver and kidney tissues exposed to CAPE. However, treatment with MEL demonstrated positive effects. MEL administration alleviated oxidative stress, reduced levels of liver enzymes, BUN, and creatinine, and ameliorated histopathological degenerations. MEL also increased GPx and TAC levels. Moreover, MEL treatment aided in restoring the body weight that was lost due to CAPE exposure.

CONCLUSION:

Our findings indicated that the administration of MEL in rats significantly enhanced the hepatic and renal toxicity induced by CAPE.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Melatonina / Antioxidantes Límite: Animals Idioma: En Revista: Hum Exp Toxicol Asunto de la revista: TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Melatonina / Antioxidantes Límite: Animals Idioma: En Revista: Hum Exp Toxicol Asunto de la revista: TOXICOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Irán Pais de publicación: Reino Unido