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Effect of metformin on clastogenic and biochemical changes induced by adriamycin in Swiss albino mice
A M Aleisa1, S S Al-Rejaie, S A Bakheet
1Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Abstract:
Diabetes mellitus (DM) is a chronic disease that is characterized by deteriorating glycemic control. The disease is known to be caused by imbalance between reactive oxygen species (ROS) and antioxidant defense systems. Hyperglycemia is commonly observed in a wide variety of diseases, including cancer. Although, therapy against glycemic control, is used in all these diseases, the diabetic cancer patients are on additional therapy with anticancer drugs. The objective of present study was to study if Glucophage (metformin), a very popular antidiabetic agent can avert the mutagenicity and lipid peroxidation caused by adriamycin (ADR), which is a commonly used cytotoxic drug. The experimental protocol included oral treatment of mice with different doses (62.5, 125 and 250 mg/kg day) of metformin for 7 days. Some mice in each group were injected i.p. with ADR (15 mg/kg). In each case animals were killed, 30 or 24, 48 and 72 h after the last treatment and femurs were excised for cytological studies by micronucleus test. Additional experiments on estimation of glutathione (GSH) and malondialdehyde (MDA) were undertaken in blood and serum, respectively. Twenty-four hour after the treatment, blood from each mouse was collected from heart and preserved for analysis. The results obtained revealed that pretreatment with metformin: (i) reduced the ADR-induced frequency of micronuclei without any alteration in its cytotoxicity and (ii) protected against the ADR-induced increase and decrease of MDA and GSH, respectively. The exact mechanism of action is not known, however, the inhibition of ADR-induced clastogenicity and lipid peroxidation by metformin may be attributed to the antioxidant action of the latter. Our results demonstrate that metformin might be useful to avert secondary tumor risk by decreasing the accumulation of free radicals and inhibition of mutagenicity.
Insights
Metformin, an antidiabetic drug, reduced mutagenicity and lipid peroxidation caused by the chemotherapy drug adriamycin in mice. This suggests metformin may help prevent secondary cancer risks by acting as an antioxidant.
Area of Science:
- Biomedical Science
- Pharmacology
- Oncology
Background:
- Diabetes mellitus (DM) involves glycemic control issues and an imbalance of reactive oxygen species (ROS) and antioxidants.
- Hyperglycemia is common in diseases like cancer, where diabetic patients receive combined treatments.
Purpose of the Study:
- To investigate if metformin (Glucophage), an antidiabetic agent, can prevent mutagenicity and lipid peroxidation induced by adriamycin (ADR), a cytotoxic drug.
Main Methods:
- Mice were orally treated with metformin (62.5-250 mg/kg) for 7 days before ADR injection.
- Cytological studies (micronucleus test) and biochemical analyses (glutathione and malondialdehyde levels) were performed.
Main Results:
- Metformin pretreatment reduced adriamycin-induced micronuclei frequency without affecting cytotoxicity.
- Metformin protected against adriamycin-induced changes in malondialdehyde (MDA) and glutathione (GSH) levels.
Conclusions:
- Metformin's antioxidant action may inhibit adriamycin-induced mutagenicity and lipid peroxidation.
- Metformin could potentially reduce secondary tumor risk by decreasing free radical accumulation and inhibiting mutagenicity.
