Biochemical toxicity induced by tramadol administration in male rats

Tramadol is a centrally acting analgesic used for treatment of moderate to severe pain. There has been some controversy regarding the dependence lability of long- term use of this medication. The present work was conducted to assess the biochemical toxicity profiles of tramadol during therapeutic use. Liver and kidney functions, sex hormones activity and some metabolic parameters were studied in male rats. Rats were divided into three groups. Group one received vehicle [saline], group two and three received oral doses of tramadol equal to 40 mg and 80 mg / kg body weight / day respectively for a month followed by 10 days recovery period. Biochemical measurements were carried out every 10 days. There was significant increase in the levels of serum aminotransferases [ALT, AST], lactate dehydrogenase [LDH], urea nitrogen [BUN], creatinine and lipid peroxide [MDA] in both tramadol groups. In contrast, serum glucose, total cholesterol and triglycerides were significantly reduced. Tramadol significantly reduced serum luteinizing hormone [LH], follicle stimulating hormone [FSH], testosterone and cortisol, but elevated prolactin [PRL] and estradiol [E[2]] in male rats specially at 20 and 30 days of treatment. After 10 days recovery, 80 mg tramadol group remained significantly different compared to control one. The present finding pointed out the risk of increased lipid peroxidatin, hepatic and renal damage and sexual dysfunction. Tramadol toxic effects should be kept in mind during long term therapy specially in large doses

Some biochemical changes induced by cyanide intoxication during smoke inhalation

Cyanide poisoning is a major factor that contributes to death due to smoke inhalation. The aim of the current study is to explore the postmortem stability of cyanide concentration in blood and tissues of fire victims and to evaluate the relation between glucose, lactate, anion gap and acute cyanide poisoning in smoke inhalation. For this purpose 30 rats exposed to combustion products cotaining HCN for 1hour were used as the animal model. Biochemical data were obtained by measuring cyanide [CN-] concentration, carboxyhemoglobin [COHb] saturation, glucose, lactate, and anion gap levels in dead rats and living ones before and after treatment as well as by measuring CN -, COHb and lactate in fire victims specimens. Results showed a slight reduction in COHb saturation and a significant decrease in cyanide concentration in postmortem blood and tissues of rats during 24 hours to 3 days when left at 25-30C compared to zero time. There was a differential disposition of inhaled HCN, with the highest tissue levels found in the lung, brain, liver and spleen in decreasing order. Postmortem lactate [blood, lung, brain, and liver] of rats was elevated with respect to time and temperature with disappearance of glucose. From stability data, it was suggested that about 50% and 100% of the original blood cyanide disappeared during 24 hours and 3 days respectively, while about 14% remained in lung and brain at 3rd day. On the other hand, results revealed the close correlation between anion gap, lactic acidosis and whole blood cyanide levels in smoke inhalation-induced cyanide poisoning. The serial blood lactate measurements are useful in predicting survival in fire victims with severe smoke inhalation