Related Experiment Video

Updated: May 11, 2026

Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products
05:27

Gap Junctional Intercellular Communication: A Functional Biomarker to Assess Adverse Effects of Toxicants and Toxins, and Health Benefits of Natural Products

Published on: December 25, 2016

The protective effects of methyl jasmonate against adriamycin--induced hepatic and renal toxicities

A M Kosoko1, C J Molokwu, E O Farombi

  • 1Drug Metabolism and Toxicology Research Laboratories, Department of Biochemistry, Faculty of Basic Medical Sciences, (IAMRAT), College of Medicine, University of Ibadan, Ibadan, Nigeria.

African Journal of Medicine and Medical Sciences
|May 18, 2013
PubMed

Insights

Methyl jasmonate (MJ) protects against adriamycin (ADR) induced liver and kidney damage by reducing oxidative stress. MJ treatment significantly improved antioxidant levels and reduced markers of toxicity in mice.

Area of Science:

  • Biochemistry
  • Toxicology
  • Pharmacology

Background:

  • Adriamycin (ADR) is a potent chemotherapy agent with significant hepatic and renal toxicities.
  • Oxidative stress plays a crucial role in ADR-induced organ damage.
  • Methyl jasmonate (MJ) is a plant-derived compound with known antioxidant properties.

Purpose of the Study:

  • To investigate the protective effects of methyl jasmonate (MJ) against adriamycin (ADR) induced liver and kidney toxicities.
  • To evaluate the impact of MJ on oxidative stress markers in ADR-treated mice.
  • To determine the optimal dosage of MJ for mitigating ADR-induced organ damage.

Main Methods:

  • BALB/c mice were divided into control, ADR, MJ-only, and MJ + ADR groups.
  • Mice received varying doses of MJ and/or ADR over an 8-day period.
  • Liver, kidney, and serum samples were analyzed for malondialdehyde (MDA), glutathione (GSH), H2O2, superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), urea, creatinine, AST, and ALT levels.

Main Results:

  • ADR treatment significantly increased MDA, H2O2, and GST, while decreasing GSH, CAT, and SOD in liver and kidney tissues.
  • MJ pretreatment significantly reduced ADR-induced increases in serum urea, ALT, MDA, H2O2, and GST.
  • MJ pretreatment also significantly elevated GSH, CAT, and SOD levels in organ tissues, indicating reduced oxidative stress.

Conclusions:

  • Methyl jasmonate (MJ) demonstrates a significant protective effect against adriamycin (ADR)-induced hepatic and renal toxicities.
  • The protective mechanism of MJ likely involves the inhibition of tissue peroxidative damage and enhancement of antioxidant defense systems.
  • MJ holds potential as a therapeutic agent to mitigate the side effects of ADR chemotherapy.

More Related Videos

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions06:32

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions

Published on: June 13, 2025

Related Concept Videos

Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
Drug Toxicity: Overview01:00

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...