Subchronic dermal exposure to T-2 toxin produces cardiac toxicity in experimental Wistar rats.

Our study aimed to determine the cardiac toxicities of T-2 toxin, a representative mycotoxin that frequently contaminates maize, cereals, and other agricultural products, harvested and stored under damp and cold conditions. Dermal exposure to T-2 toxin caused severe cardiotoxicity in experimental Wistar rats. Electrocardiography studies showed the conduction abnormalities including prolongation of the QT and corrected QT interval, shortening of the PR interval, and tachycardia. Biochemical studies also reported the toxicity of T-2 toxin. T-2 toxin induced acute cardiotoxicity in rats and characterized by significant (p < 0.05) elevation of serum troponin I, creatine kinase (CK) isoenzyme MB, CK isoenzyme NAC, and lactate dehydrogenase as compared to control rats. It is concluded that cardiotoxicity effects of T-2 toxin are thought to be due to direct action on electrocardiac potentials and biochemical changes.

Acute and subchronic dermal toxicity of Vitex negundo essential oil.

Vitex negundo is a common herb in different herbal formulation. The potential acute and sub-chronic dermal toxicities were evaluated as per OECD (Organization for Economic Cooperation and Development) guidelines 402 and 411, respectively. Both sexes of Wistar rats were exposed to Vitex negundo oil of 2000 mg/kg body weight for acute dermal toxicity, whereas in the dermal sub-chronic toxicity study, rats were exposed to Vitex negundo oil 250, 500 and 1000 mg/kg body weight, respectively, for five times a week for 90 d. In acute and sub-chronic toxicity studies, all animals were normal without any behavioral, serum biochemistry, hematology, necroscopical and histopathological changes. The no observed effect level (NOEL) and no observed adverse effect level (NOAEL) of Vitex negundo oil were 250 and 1000 mg/kg/day, respectively. Vitex negundo oil is under the category 5 (Unclassified) according to the Globally Harmonized System, with an LD50 value of over 2000 mg/kg.

Synergism of ochratoxin B and calcium-channel antagonist verapamil caused mitochondrial dysfunction.

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.

Comparative hematoxicity of fusirium mycotoxin in experimental sprague-dawley rats.

Mycotoxins are fungal toxin and contaminated to human through food-stuffs. Hematological abnormality, mainly thrombocytopenia and leukopenia are induced after consumption of mycotoxin. Experiments were conducted to evaluate the hematotoxicity of trichothecenes mycotoxins in Sprague-Dawley rats. Hematological parameters viz. Hemoglobin, hematocrit, erythrocyte count (RBC), white blood cell count (WBC), lymphocytes, monocytes, neutrophils, eosinophils, basophils, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red blood cell distribution width, mean platelet volume, plateletcrit and platelet distribution width were determined at 0, 6, 12 and 24 h after injection of 0.5 ml of T-2, Deoxynivalenol (DON), nivalenol, zearalenone, neosolaniol, ochratoxin-B mycotoxin equivalent to 1 × 10(-3) µg/µl to Sprague-Dawley rats. Experiments showed that trichothecenes toxin produces severe hematological alternation. The reductions of RBC and WBC were observed in all Fusarium mycotoxins treated group. T-2 toxin group shows severe toxicity as compared to other mycotoxin treated group. DON is the least hematotoxicity and T-2 the most.

Incidence and pattern of maxillofacial trauma due to road traffic accidents: a prospective study.

BACKGROUND: The incidence and causes of road traffic accidents (RTAs) vary with geographical location, socioeconomic status, religion and era. The etiological factors and associated injury patterns may be important in planning for preventive measures and treatment planning. The aim of this study was to evaluate and analyze the etiological factors, patterns and the frequency of maxillofacial injuries due to RTAs. MATERIALS AND METHODS: This prospective study was conducted on 350 patients with facial trauma due to RTAs. Records related to age, sex, the cause of the RTA, the vehicle type, time to reach the hospital, the use of seat belts, helmets, and other safety devices were evaluated and reviewed. RESULTS: Two-wheelers were the most involved (53.71 %) vehicle type and negligence of traffic rules (24 %) was the most common etiological factor. Male to female ratio was 6.3:1. The age group of 21-50 (68.85 %) years was mostly affected. The nasal bone (29.14 %) was most often the site of fracture followed by mandible (28.0 %). The rate of accident was higher during 1000-1400 hours (23.14 %) period and during weekends (38.0 %). Majority (58.57 %) of victims reached the hospital within 6 h of accident. CONCLUSION: The low utilization of safety devices like seat belts and helmets as well as speeding, negligence of traffic rules and reckless driving were identified as etiological factors.