Florfenicol, as a replacement for chloramphenicol, can tightly bind to the A site of the 23S rRNA in the 50S subunit of the 70S ribosome, thereby inhibiting protein synthesis and bacterial proliferation. Due to the widespread use in aquaculture and veterinary medicine, florfenicol has been detected in the aquatic environment worldwide. Concerns over the effects and health risks of florfenicol on target and non-target organisms have been raised in recent years. Although the ecotoxicity of florfenicol has been widely reported in different species, no attempt has been made to review the current research progress of florfenicol toxicity, hormesis, and its health risks posed to biota. In this study, a comprehensive literature review was conducted to summarize the effects of florfenicol on various organisms including bacteria, algae, invertebrates, fishes, birds, and mammals. The generation of antibiotic resistant bacteria and spread antibiotic resistant genes, closely associated with hormesis, are pressing environmental health issues stemming from overuse or misuse of antibiotics including florfenicol. Exposure to florfenicol at μg/L-mg/L induced hormetic effects in several algal species, and chromoplasts might serve as a target for florfenicol-induced effects; however, the underlying molecular mechanisms are completely lacking. Exposure to high levels (mg/L) of florfenicol modified the xenobiotic metabolism, antioxidant systems, and energy metabolism, resulting in hepatotoxicity, renal toxicity, immunotoxicity, developmental toxicity, reproductive toxicity, obesogenic effects, and hormesis in different animal species. Mitochondria and the associated energy metabolism are suggested to be the primary targets for florfenicol toxicity in animals, albeit further in-depth investigations are warranted for revealing the long-term effects (e.g., whole-life-cycle impacts, multigenerational effects) of florfenicol, especially at environmental levels, and the underlying mechanisms. This will facilitate the evaluation of potential hormetic effects and construction of adverse outcome pathways for environmental risk assessment and regulation of florfenicol.

Chloramphenicol antibiotics are widely applied in human and veterinary medicine. They experience natural attenuation and/or chemical degradation during oxidative water treatment. However, the environmental risks posed by the transformation products of such organic contaminants remain largely unknown from the literature. As such, this review aims to summarize and analyze the elimination efficiency, reaction mechanisms, and resulting product risks of three typical chloramphenicol antibiotics (chloramphenicol, thiamphenicol, and florfenicol) from these transformation processes. The obtained results suggest that limited attenuation of these micropollutants is observed during hydrolysis, biodegradation, and photolysis. Comparatively, prominent abatement of these compounds is accomplished using advanced oxidation processes; however, efficient mineralization is still difficult given the formation of recalcitrant products. The in silico prediction on the multi-endpoint toxicity and biodegradability of different products is systematically performed. Most of the transformation products are estimated with acute and chronic aquatic toxicity, genotoxicity, and developmental toxicity. Furthermore, the overall reaction mechanisms of these contaminants induced by multiple oxidizing species are revealed. Overall, this review unveils the non-overlooked and serious secondary risks and biodegradability recalcitrance of the degradation products of chloramphenicol antibiotics using a combined experimental and theoretical method. Strategic improvements of current treatment technologies are strongly recommended for complete water decontamination.

The presence of residues from frequent antibiotic use in animal feed can cause serious health risks by contaminating products meant for human consumption such as meat and milk. The present paper gives an overview of the electrochemical methods developed for the detection of phenicol antibiotic residues (chloramphenicol, thiamphenicol, and florfenicol) in different kinds of foodstuffs. Electrochemical sensors based on different biomolecules and nanomaterials are described. The detection limit of various developed methods with their advantages and disadvantages will be highlighted.

Chloramphenicol has certain notable characteristics: it penetrates reliably into the central nervous system; it is usually bacteriostatic, but is bactericidal for Hemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis; it is metabolized in the liver, and levels of drug in serum need to be monitored in patients with liver disease and in neonates. Potential toxicity limits the use of this drug. It has been estimated that death from aplastic anemia occurs in oe of 24,500-40,800 courses of treatment. The incidence of aplastic anemia after parenteral therapy is unknown; however, only a few cases have been reported. The gray baby syndrome occurred in premature and newborn infants receiving high or unmodified doses of chloramphenicol. This condition can be avoided by reduction of dosage and by monitoring levels of drug in the serum of these infants. The most common toxicity is a reversible, dose-related bone marrow suppression, which is identified by serial monitoring of reticulocyte and complete blood cell counts. Many of the indications for use of this drug are still controversial because studies comparing the toxicity and efficacy of chloramphenicol and of alternative antibiotics have not been done.

This article reviews specific aspects of the pharmacokinetics and clinical toxicity of thiamphenicol. Studies on the systemic bioavailability in humans of 2.5 g of thiamphenicol given orally showed mean peak levels in plasma of 16.1-18.6 micrograms/ml after about 2 hr, and plasma concentrations of thiamphenicol of greater than 2 micrograms/ml for approximately 17-20 hr. The oral dose of 2.5 g appeared no less bioavailable than the usual 0.5-g parenterally administered dose. The distribution of thiamphenicol to selected urogenital tissues is also summarized. Clinical data on toxicity obtained during 1980-1982 confirmed that thiamphenicol does possess a hematopoietic suppressant potential of the dose-related type, which appeared to be observed only after repeated dosing. On the other hand, thiamphenicol does not appear to be associated with the dose-unrelated, delayed type of hemotoxicity known to occur after therapy with chloramphenicol.

Until the last few years, chloramphenicol was recognized positively as the drug of choice in the treatment of acute typhoid fever. Its hematoxicity, as well as the recently observed epidemic and the present endemic occurrence of S. typhi strains with R-factor-mediated resistance to chloramphenicol in Mexico, India and South-EAst Asia, render the clinical evaluation of new antibacterial agents extremely important. By means of a literature review on controlled comparative trials, the value of thiamphenicol, ampicillin, amoxycillin, furazolidone and co-trimoxazole as alternative drugs for the treatment of acute typhoid fever is examined. Co-trimoxazole seems to be the drug of choice in the treatment of acute typhoid fever. For the treatment of the chronic typhoid carrier ampicillin is most frequently used, but amoxycillin and co-trimoxazole seem to be just as effective.