Ochratoxin A Toxicity in Rabbits—A Review
Ochratoxin A (OTA), a mycotoxin produced by Aspergillus and Penicillium species, is a widespread feed contaminant with nephrotoxic, hepatotoxic, immunotoxic, reproductive, and teratogenic effects. Despite the particular susceptibility of rabbits to OTA, information on ochratoxicosis in this species remains limited. This review summarizes current evidence on OTA occurrence, toxicokinetics, mechanisms of toxicity, clinicopathological effects, immunotoxicity, and preventive strategies in rabbits. Following gastrointestinal absorption, OTA has a high affinity for plasma proteins and preferentially accumulates in the kidneys and liver. Its toxicity is mediated by the inhibition of protein synthesis, mitochondrial dysfunction, oxidative stress, genotoxicity, apoptosis, and immune dysregulation, ultimately leading to renal and hepatic injury, hematological and biochemical alterations, impaired growth, and reproductive toxicity. OTA-induced immunosuppression may also increase susceptibility to secondary infections, including Pasteurella multocida. Importantly, pathological and biochemical alterations may occur following relatively low-level exposure, while residual OTA levels may persist in tissues after exposure is discontinued. Effective prevention of OTA contamination in feed is therefore crucial for controlling ochratoxicosis. Microbial and enzymatic detoxification, probiotics, and phytogenic additives represent promising approaches for the prevention and mitigation of OTA toxicity; however, further studies in rabbits are needed to establish their efficacy and optimal application and to evaluate the effects of different OTA doses, early biomarkers, and tissue residue kinetics.
Authors
- Kalina Zhivkova (ORCID: https://orcid.org/0009-0000-9523-4456)
Institutions
- Trakia University (BG)
Publication Details
- Journal
- Toxins
- Published
- 2026-09-28
- DOI
- https://doi.org/10.3390/toxins18100415
- Primary Topic
- Mycotoxins in Agriculture and Food
- Type
- article
- Field-Weighted Citation Impact
- 0.00