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This study aimed to assess the acute toxicity in rats of heated and un heatedbutylated hydroxytoluene (BHT). Sunflower oil dissolved BHT, heated at 98±2ºC by a water bath. The animals were divided into five groups. The control group dosage orally with sunflower oil, the first group treated with 250 mg/kg BHT, the second group treated with 250 mg/kg heated, BHT the third group treated with 500 mg/kg BHT and the fourth group treated with 500 mg/kg heated BHT. All groups received oral treatment. The results showed a substantial reduction in motor activity relative to other groups at a dose of 250 mg/kg heated BHT. There was a substantial distinction in the negative geotaxis test in groups of 500 mg/kg heated and un-heated BHT, while a cliff avoidance test in the heat treated dose of 250 and 500 mg/kg was observed in the cliff avoidance test compared to other groups. A significant reduction occurred in all groups in the pocketing and dorsal tonic immobility test. The pathological changes of heated BHT groups were more severe than those of un-heated BHT groups especially the dose of 500 mg/kg heated BHT. It represented by coagulative necrosis, muscle atrophy in heart, interstitial pneumonia, serofibrinous exudate, pulmonary emphysema in lung and neuronal degeneration, microgliosis, myelin vacuolation and satellitosis in the brain. The study concluded that heated BHT at a dose of 250 and 500 mg/kg had toxic effects to motor and neurobehavioral activity, and histopathological changes in the brain, heart, and lung.

This study investigated the Pharmacokinetics of ciprofloxacin alone or with diclofenac sodium in adult Japanese quails. The quails divided into two groups, the first group was dosed intraperitoneally with 50 mg/kg of ciprofloxacin, the second group was injected by 50 mg/kg of ciprofloxacin intraperitoneally then directly injected intraperitoneally by diclofenac sodium at a dosage of 5 mg/kg. Plasma concentrations of ciprofloxacin were determined by the spectrophotometer at wavelength 290 nm. Co-admiration of ciprofloxacin with diclofenac lead to appearing ciprofloxacin in plasma at 12.02, 6.4, 5.3, 3.30, 1.36, 0.60 μg/ml in the periods of 0.25, 0.50, 1, 2, 4 and 8 hours post-injection. A significantly increased in the concentration of ciprofloxacin at times of 0.25, 0.50, 1, and 2 hours post-injection and appeared at a concentration of 6.96, 3.09, 2.2, and 0.72 μg/ml. The pharmacokinetics of ciprofloxacin when given with diclofenac sodium was represented by 91% decrease in elimination constant rate, 53% decrease in elimination half-life t1/2, 64% decrease in volume of distribution to steady-state, 22% decrease in clearance, 28% increase area under curve, 41% decrease in area under moment curve, 53% decrease in mean residence time and 37% increase in maximum plasma concentration. Our study concludes that co-administration of ciprofloxacin with diclofenac sodium lead to alteration in some pharmacokinetic data of ciprofloxacin like effect on the plasma concentration and volume of distribution and clearance. This effect must be considered when therapy by ciprofloxacin with diclofenac, the co-administration of diclofenac with ciprofloxacin decrease the elimination of ciprofloxacin.

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The aim of this study to explore the therapeutic effect of boric acid on the neurobehavioral (motor activity) level, and histopathologic changes in the brain, liver and kidneys against fluorosis. In this study rose chicks have been used and determined medium lethal sodium fluoride dose at 346.5 mg/kg orally. The chicks divided into four random groups each one consists of 10 chicks. The first group considered to be a control group, the second received 20 mg/kg of sodium fluoride, the third group received 10 mg/kg of boric acid and the fourth received 20 mg/kg of sodium fluoride and boric acid at the same previous dosages. After two weeks of daily treatment, neurobehavioral measures were taken, the use of boric acid has a major effect to improve the neurobehavioral measurement and develop complications of ALT, AST, creatinine, Ca, MDA. The results indicate that boric acid may be a therapeutic agent against the fluoride toxicity of the brain, liver and kidney. This result support by histopathological changes which represented by inflammation, congestion of portal vein and dilation of sinusoids in the liver and vacuolation, vasogenic edema and gliosis in the brain and Kidney of showed segmentation of glomeruli, dilation of Bowman's space, necrosis of epithelial cells renal tubules and hemorrhage of NaF group, while the liver of the NaF with boric acid group showed an improvement the results of histopathological examination of the liver, brain and kidneys compared to the NaF group alone. The results revealed that boric acid has a preventing effects against fluoride after two weeks of treatment with boric acid.