Chloramphenicol, a broad-spectrum antibiotic initially identified in 1947 from the soil bacterium Streptomyces venezuelae, gained widespread use in treating various bacterial infections, including typhoid fever, due to its ability to penetrate tissues and fluids effectively. Approved by the U.S. Food and Drug Administration in 1948, it became one of the first antibiotics of its kind, significantly impacting medical treatment in the mid-20th century. Chloramphenicol's broad antibacterial activity enabled its use in treating infections like acute bronchitis and even certain viral infections during the 1950s. However, its popularity waned in the 1960s following the identification of its toxic effects on bone marrow, specifically causing aplastic anaemia and dose-dependent toxicity, which can lead to reversible anaemia if the medication is discontinued. Another severe side effect, the "grey syndrome," was noted in neonates exposed to the drug, further limiting its use. This study explores the long-term effects of chloramphenicol on liver and kidney function, as well as its impact on oxidative stress markers, using a rodent model (Sprague-Dawley rats). The research aims to provide further understanding of the potential hepatotoxic and nephrotoxic effects of chronic chloramphenicol administration, contributing to a more comprehensive safety profile for its use in clinical settings. The findings underscore the need for continued caution in the use of chloramphenicol, particularly in vulnerable populations, and advocate for more targeted treatment strategies that minimize adverse health risks.