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Anti-plasmodial activity of sodium acetate in Plasmodium berghei-infected mice

  • Adam O. Abdulkareem EMAIL logo , Abdulkareem O. Babamale , Lucky O. Owolusi , Simbiat A. Busari and Lawrence A. Olatunji
Published/Copyright: April 10, 2018

Abstract

Background

Continuous increase in drug resistance has hindered the control of malaria infection and resulted in multi-drug-resistant parasite strains. This, therefore, intensifies the search for alternative treatments with no or less side effects. Several histone deacetylase inhibitors have been characterised to possess anti-malaria activity; however, their further development as anti-malaria agents has not recorded much success. The present study investigated the anti-plasmodial activity of sodium acetate in Plasmodium berghei-infected mice, aiming at finding a better alternative source of malaria chemotherapy.

Methods

Thirty female Swiss albino mice were randomly distributed into six groups. Groups A (uninfected control) and B (infected control) received only distilled water. Group C (artesunate control) were infected and treated orally with 4 mg/kg artesunate on the first day, and subsequently 2 mg/kg artesunate. Groups D, E and F were infected and orally treated with 50, 100 and 200 mg/kg sodium acetate, respectively.

Results

Sodium acetate significantly lowered parasitaemia (p<0.05) after 4 days post-treatment, and the parasite inhibition rate of 68.5% at 50 mg/kg compared favourably with the 73.3% rate of artesunate. Similarly, administration of 50 mg/kg sodium acetate improved serum total cholesterol relatively better than artesunate. Our results also revealed that sodium acetate does not interfere with liver function, as there was no significant difference (p>0.05) in the serum activities of aspartate aminotransferase and alanine aminotransferase in both infected treated and uninfected mice.

Conclusions

This study shows that sodium acetate may be a safe alternative source of anti-malaria drugs. Its effect on the serum total cholesterol also predicts its ability in correcting malaria-induced metabolic syndromes.

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: None declared.

  3. Employment or leadership: None declared.

  4. Honorarium: None declared.

  5. Competing interests: The funding organisation(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2017-11-27
Accepted: 2018-02-23
Published Online: 2018-04-10
Published in Print: 2018-09-25

©2018 Walter de Gruyter GmbH, Berlin/Boston

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