Evaluates hepatorenal toxicity and oxidative stress in response to chloramphenicol, suggesting risks of prolonged use.
Chloramphenicol is a broad-spectrum antibiotic first discovered in 1947 from the soil microorganism Streptomyces venezuelae and later approved for clinical use following its effectiveness in treating typhoid fever outbreaks. Its extensive antibacterial activity and high tissue permeability contributed to its widespread use in the mid-20th century for the treatment of various bacterial and some viral-associated conditions. However, concerns regarding its safety profile, particularly its association with severe adverse effects such as aplastic anaemia and dose-dependent bone marrow suppression, led to a decline in its clinical application. This study evaluates the hepatorenal and oxidative stress responses associated with chronic exposure to chloramphenicol. Given its known toxicity, prolonged use may disrupt normal physiological functions, especially in the liver and kidneys, which are primary sites for drug metabolism and excretion. Additionally, oxidative stress has been implicated as a key mechanism underlying drug-induced organ damage, resulting from an imbalance between reactive oxygen species production and antioxidant defense systems. Chloramphenicol is chemically identified as D-(-)-threo-1-p-nitrophenyl-2-dichloroacetamido-1,3-propanediol, a neutral, crystalline compound that is soluble in alcohol but poorly soluble in water. Among its four stereoisomers, the D-erythro form is primarily responsible for its antibacterial activity, exhibiting approximately 98% efficacy, whereas the L-erythro isomer demonstrates minimal activity. Despite its therapeutic benefits, esterified derivatives such as succinate and palmitate have shown limited antimicrobial effectiveness. The present study aims to provide insight into the toxicological implications of chronic chloramphenicol exposure, with particular emphasis on its effects on hepatic and renal function as well as oxidative stress biomarkers. Understanding these effects is essential for evaluating the risks associated with its prolonged use and for guiding safer therapeutic applications.
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Okoye et al. (2026) studied this question.
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