Association of plasma level of thiobarbituric acid reactive substances with extent of hepatocellular injury in preterm infants with cholestatic jaundice

The present study was designed to determine the association between extent of hepatocellular injury and plasma level of thiobarbituric acid reactive substances (TBARS) in pre term infants with cholestasis. Preterm infants (<35 weeks gestation) admitted to the neonatal intensive care unit were enrolled (with their parents informed consent) in either the ‘cholestasis’ group (if their direct bilirubin was >2 mg/dl) (n=25) or in the control group (n=16). Blood samples for measurement of TBARS, direct bilirubin and transaminases were obtained with-in 24 hours of enrollment. The cholestasis and control groups were comparable with respect to gestational age, birth weight and Apgar score. Serum direct bilirubin, SGOT (EC 2.6.1.1) and SGPT (EC 2.6.1.2) levels were significantly high in the cholestasis group. Plasma levels of TBARS in cholestasis group were correlated with SGOT (F=276.92; P<0.0001) and SGPT (F=355.17; P<0.0001) and differed significantly between cholestatic and control infants. Our findings suggest that oxidative stress in preterm infants with cholestasis is associated with hepatocellular injury.     

Serum enzymes in thermal injury

Various metabolic and biological changes follow burn injury. Serum Thio-barbituric acid reactive substances (TBARS), transaminases, alkaline phosphatase and amylase were measured in 43 patients with thermal injury over the first 10 days of post burn period. No clear correlation between elevated serum enzymes except amylase and the burn size was observed on admission. Mean serum TBARS were significantly increased in the burn patients. Transaminases values increased till 5^th day then declined on 10^th day, whereas alkaline phosphatase and amylase activities continued to rise till day 10. It is concluded that functional disturbances occur in liver and pancreas around a week after thermal injury. Monitoring serum ALP and amylase in postburn period has valuable prognostic importance.     

Role of ethanol on aluminum induced biochemical changes on rat brain

Aluminum and alcohol, both are well-accepted neurotoxin. The plausible mechanisms for their neurotoxicity are also common. Therefore, the effect of ethanol on aluminum induced biochemical changes in rat brain is being studied. In the present study, ethanol exposure significantly affected the aluminum and protein content of brain. The activities of acid phosphatase and alkaline phosphatase were also changed. Aluminum exposure, on the other hand, contributed significantly in the alterations of aluminum content, acid phosphatase acivity and aspartate aminotransferase activity. Though ethanol co-exposure significantly influenced the aluminum load of brain, the interactions of these two neurotoxins were found to be significant only in case of acid phosphatase activity of brain. Therefore, it can be suggested that general neurotoxicity produced by aluminum is not modified by ethanol. However, the aluminum load caused by aluminum exposure, may be influenced by ethanol co-exposure.     

金樱子多糖对免疫抑制小鼠肝功能及血脂代谢的调节作用

为探讨金樱子多糖对免疫抑制小鼠肝功能及血脂代谢的调节作用,取50只昆明小鼠随机平均分为正常对照组、模型组、RLP低剂量组、RLP中剂量组、RLP高剂量组．低、中、高剂量组分别按100ms／kg·d、200mg／kg·d、400mg／kg·d连续灌胃30d;正常对照组和模型组灌胃生理盐水．于试验前一周在继续灌胃的基础上,除正常对照组外,分剐于第l、3、5天给小鼠按25mg／kg体重腹腔注射地塞米松（Dex）建立免疫抑制动物模型．摘小鼠眼球取血,用试剂盒测定小鼠血清的总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL—C）、低密度脂蛋白胆固醇（LDL—C）、谷草转氨酶（AST）、谷丙转氨酶（ALT）．结果表明,金樱子多糖能显著降低免疫抑制小鼠血清中TC、LDL—C、AST、Au含量,对HDL—C和TG有一定的调节作用．因此,金樱子多糖对免疫抑制小鼠肝功能及血脂代谢具有一定的调节作用．