-Context -Zearalenone is a mycoestrogen and considered a mycotoxin. Objective -To establish whether zearalenone produced hepatotoxicity via oral administration. Methods -Zearalenone was orally administered at a dose of 50 μg, 100 μg and 200 μg ZEN/ body weight/daily, respectively, for 14 days to three groups of BALB/c mice. Diagnostic modalities used to evaluate hepatic damage and impaired hepatic function pre-and post zearalenone administration included hepatic marker enzyme activity, pentobarbital sleeping time, cytochrome P-450 activities and histopathologic evaluation of liver. Results -Significant histopathologic changes viz. sinusoidal congestion, cytoplasmic vacuolization, hepatocellular necrosis and neutrophil infiltration were observed after evaluating of liver section from each group after accumulated zearalenone exposure. Further, zearalenone exposure increased activities of alanine transaminase, aspartate transaminase and lipid peroxides whereas activities of tissue glutathione and cytochrome P 450 were decreased as compared to control mice. Zearalenone also increased the sleeping time and decreased sleeping latency after pentobarbital through intraperitoneal route as compared to control mice which indicates that the impairment of hepatic metabolizing enzymes by zearalenone. Conclusion -Zearalenone is a potential hepatotoxin by oral route. Headings -Zearalenone. Hyperplasia. Liver, pathology. Mice.

rapid and severe when drug administration is suspended and re-challenged. NVP induced rash has been reported in 4.3-36% of adults [3] with prevalence for Thai HIV patients ranging from 6% to -21%. [4] In Sardinian population were HLA B14 and Cw8 was associated 26% developed NVP induced rash, in our study from India we found that NVP-induced rash was 2.14%, thus, refl ecting the comparatively a high incidence of drug-related rash in Asians. [5] Recent studies have shown that hypersensitivity reactions to antiretroviral drugs are HLAassociated. HIV-infected Thai patients have a signifi cant HLA Cw*04 allele association with nevirapine induced rash cases. [4] HLA B*3505 allele has been identifi ed as a strong predictor for nevirapine-induced skin adverse reactions in Thai HIV patients. [6] This study shows that HLA B35 is signifi cantly associated among the nevirapine-induced skin rash HIV-1 ARV-treated patients of India. Further, the molecular HLA characterization of these alleles will enlighten us on the immunological basis of the antiretroviral drug reactions.

We examined the mechanism by which the ochratoxin B induced interaction with calcium-channel antagonist verapamil and mitochondrial dysfunction of the rat trachea in vitro experiment. The tracheas were cut into 2-3 mm wide rings and suspended in a tissue bath. Isometric tension was continuously measured with an isometric force transducer connected to a computer-based data acquisition system. Verapamil (1 × 10(-6) M) produced a concentration-dependent contraction response in rat's tracheal rings pre-contracted by acetylcholine. Incubation of rat's tracheal rings with the ochratoxin B significantly potentiated the contraction responses of verapamil. Verapamil and OTB accelerate the overloading of Ca(2+) in tracheal smooth muscle contributes the tissue toxicity as shown in electron microscopy and mitochondrial enzymes, through a mechanism that could involve perturbations of Ca(2+) homeostasis. These results proved that ochratoxin B is a potential vasoconstrictor mycotoxin with the presence of calcium-channel antagonist. In conclusion, disturbance of Ca(2+) homeostasis caused by OTA and plays a significant role in produces toxicity through mitochondrial enzyme inhibition.