Methamphetamine-Associated Myocardial Injury and Its Modification by Vitamin E in an Experimental Rat Model

Ateen Amer Hameed 1, * and Anhar Rabeea Hussein 2

1 Medical Biotechnology Department, College of Science, Tikrit University, Iraq.
2 Biology Department, College of Science, Tikrit University, Iraq.
* Corresponding Author
ORCID Details
 
Research Article
International Journal of Biological and Pharmaceutical Sciences Archive, 2026, 12(01), 237–243.
Article DOI: 10.53771/ijbpsa.2026.12.1.0094
Publication history: 
Received on 17 August 2026; revised on 20 September 2026; accepted on 22 September 2026
 
Abstract: 
The aim of this study was to determine the toxic effects of methamphetamine with regards to the histological structure of cardiac muscle in adult male white rats, and to see whether Vitamin E could offer a protective effect against the toxic effects of methamphetamine. The study was conducted in the Animal Facility and the Laboratory of the College of Veterinary Medicine, Tikrit University from October 1st, 2025 till November 1st, 2025. Thirty-two adult male white Sprague–Dawley rats were randomly divided into 4 main groups (n=8/group), each of which was split into 2 subgroups (15- vs 30-day treatment). The control group was Group 1 while methamphetamine at a dose of 0.1 mg/kg and 1 mL/day was administered to Group 2, Vitamin E at a dose of 0.1 mL/day to Group 3 and a combination of Vitamin E 0.1 mL/day and methamphetamine 0.1 mg/kg to Group 4. Animals treated with methamphetamine exhibited hyperactivity, increased cage movement, increased agitation, and decreased food and water consumption. Hearts were removed at the conclusion of each experimental period for histopathologic analysis. Histological changes in coronary blood vessels, infiltration of inflammatory cells, hemorrhage, atrophy of myofiber with loss of nuclei and expansion of intramuscular connective tissues were observed, and lesion severity increased with the duration of exposure. The Vitamin E group also showed some minor amount of changes in the histological picture, this might be due to the dosage or length of administration. Despite the fact that methamphetamine/VE treatment was not effective at producing complete lesions, it did show a relative decrease in the severity of the lesions compared to methamphetamine alone. The researchers conclude that methamphetamine exposure causes chronic, dose-dependent toxicity to cardiac muscle, suggesting that exposure causes a slowly progressive damage to cardiac tissue. Moreover, Vitamin E provided partial protection from methamphetamine-induced cardiotoxicity but was not enough to reverse all histological changes, highlighting the importance of further research to determine an optimal dosage and elucidate the mechanism of protection in chronic methamphetamine exposure.
 
Keywords: 
Methamphetamine, Cardiotoxicity, Vitamin E, Cardioprotection, Histopathology, Myocardial Injury.
 
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