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Cytochrome P(450)-dependent toxic effects of primaquine on human erythrocytes.

Author: GanesanShobana, SahuRajnish, TekwaniBabu L, TripathiLalit M, WalkerLarry A

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.
Research Support, U.S. Gov't, Non-P.H.S.Research funding provided by US government agencies other than the Public Health Service.

Overview

Primaquine, an antimalarial drug, can cause hemotoxicity, particularly in individuals with glucose-6-phosphate dehydrogenase deficiency. This study identifies cytochrome P450 (CYP) isoforms that contribute to primaquine hemotoxicity, providing insights for potentially minimizing these adverse effects.
Paper Details　
Original Abstract of the Article :
Primaquine, an 8-aminoquinoline, is the drug of choice for radical cure of relapsing malaria. Use of primaquine is limited due to its hemotoxicity, particularly in populations with glucose-6-phosphate dehydrogenase deficiency [G6PD(-)]. Biotransformation appears to be central to the anti-infective a...See full text at original site
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引用元：
https://doi.org/10.1016/j.taap.2009.07.012

データ提供：米国国立医学図書館（NLM）

Primaquine: A Double-Edged Sword in Malaria Treatment

This research delves into the complex relationship between the antimalaria drug primaquine and its potential for hemotoxicity, a side effect that can damage red blood cells. The study investigates the role of cytochrome P(450) enzymes, a family of proteins responsible for metabolizing drugs in the body, in the detoxification and toxicity of primaquine. The researchers utilized an in vitro system to study the metabolism of primaquine by different cytochrome P(450) isoforms, revealing the specific isoforms involved in its hemotoxicity. This research provides important insights into the mechanisms underlying primaquine's toxicity and the potential for developing strategies to mitigate its harmful effects.

Metabolic Pathways and Hemotoxicity: A Delicate Balance

This research reveals the critical role of cytochrome P(450) enzymes in the metabolism and hemotoxicity of primaquine. The study identifies several specific cytochrome P(450) isoforms that are involved in the generation of toxic metabolites. This understanding paves the way for developing strategies to minimize the risk of hemotoxicity, potentially by targeting these specific isoforms or using alternative treatment regimens.

Primaquine: A Powerful Tool with Potential Risks

This research highlights the delicate balance between the therapeutic benefits and potential risks of primaquine. While this drug remains an effective treatment for malaria, its hemotoxicity poses a significant concern, particularly for individuals with glucose-6-phosphate dehydrogenase deficiency. It is crucial to consult with a healthcare professional to determine the appropriate use of primaquine and to ensure its safe and effective administration.

Dr.Camel's Conclusion

This research is a testament to the complex interplay between metabolism, genetics, and drug toxicity. The study's findings provide valuable insights into the mechanisms underlying primaquine's hemotoxicity, highlighting the importance of careful patient selection and personalized treatment strategies to optimize its therapeutic benefits while minimizing its potential risks.
Date :
  1. Date Completed 2009-11-04
  2. Date Revised 2022-03-16
Further Info :

Pubmed ID

19616568

DOI: Digital Object Identifier

10.1016/j.taap.2009.07.012

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Languages

English

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