International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Wed, Apr 29, 2026
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Abstract: (43 Views)
Introduction: Ochratoxin-A (OTA) represents one of the primary secondary metabolites produced by Penicillium and Aspergillus species. Acratoxin was recognized in 1965 as the most significant carcinogenic mycotoxin found in agricultural products. Given that the vital function of the lungs in maintaining other bodily organ system, it was examined the role of the Zataria multiflora extract in an experimental model of lung inflammation induced by Ochratoxin-A in mice.
Materials and Methods: This study was designed around a 14-day gavage administration of OTA in mice. Markers of oxidative stress and apoptotic factors (Bax/Bcl2, Caspase 3 Caspase 9) were also evaluated.
Results: OTA-induced toxicity provokes lung inflammation and apoptosis in a dose-dependent manner. The administration of Zataria multiflora (at dosages of 25 and 50 mg/kg) resulted in a significant alleviated of lung inflammation, oxidative damage, inflammatory cytokines, and levels of apoptosis protein when compared to the group treated with OTA alone.
Conclusion: The results of the study indicate that Zataria multiflora exerts robust antioxidant effects that counteract the inflammation and apoptosis associated with OTA-induced toxicity in lung tissue.
Materials and Methods: This study was designed around a 14-day gavage administration of OTA in mice. Markers of oxidative stress and apoptotic factors (Bax/Bcl2, Caspase 3 Caspase 9) were also evaluated.
Results: OTA-induced toxicity provokes lung inflammation and apoptosis in a dose-dependent manner. The administration of Zataria multiflora (at dosages of 25 and 50 mg/kg) resulted in a significant alleviated of lung inflammation, oxidative damage, inflammatory cytokines, and levels of apoptosis protein when compared to the group treated with OTA alone.
Conclusion: The results of the study indicate that Zataria multiflora exerts robust antioxidant effects that counteract the inflammation and apoptosis associated with OTA-induced toxicity in lung tissue.
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