ABSTRACT
Objective:To evaluae the unification of endoplasmic reticulum and mitochondrium in fetal rat cerebral neuron apoptosis induced by intrauterine distress. Methods:Fetal rat intrauterine distress model was established. The samples were randomly divided into normal group and ischemia-reperfusion group(IR). Expression of GRP78,caspase-9,caspase-12,and cytoron C protein were detected by western blot technique. Results:The expression of GRP78 on corresponding time in IR group was significantly higher than that in normal group. And it reached the maximum at 3h of reperfusion. The expression of GRP78 reduced step by step as reperfusion time extended. The expression of caspase-9 and caspase-12 at corresponding time in IR group were significantly higher than those in normal group. Their expression increased rapidly and reached the maximum at 12h of reperfusion. The expression of cytoron C in kytoplasm at corresponding time in IR group was significantly higher than that in normal group and reached the maximum at 12h of reperfusion. Conclusion:The synergistic effect of endoplasmic reticulum and mitochondrium plays an important role in fetal rat cerebral neuron apoptosis induced by intrauterine distress.
ABSTRACT
:Mitochondrial respiratory rate,respiratory control rate(RCR),oxidative phospho-rylation efficiency(ADP/O),and hepatic ATP content were determined in rats under 5 conditions including acute obstructive cholangitis(AOC),bile duct ligation(BDL),verapamil pretreatment in AOC(VET),dexamethasone pretreatment in AOC(DET).and sham operation(SO).It was found that rnitochondrial respiratory rate especially its state 4 phase was significantly increased and RCR,ADP/O,and ATP were significantly decreased at 6th hour after AOC and at 24th after BDL.These changes occurred earlier and more dramatically in AOC than in BDL.Pretreatment with verapamil or dexamethasone in AOC could minimize the changes of RCR,ADP/O and ATP in varying intervals.The findings indicate that AOC and BDL can both result in severe functional impairment of the mitochondria of hepatocytes and verapamil and dexamethasone exert effective protection on the rnitochondrial functions of respiration and energy metablism.
ABSTRACT
The changes of calcium and magnesium content in brain tissue (BCa;BMg) and in the mitochondria (MCa,MMg) and calmodulin content in the cortex and hippocampus (CCaM,HCaM) were determined in the rats with 4-vessel-ligation cerebral ischemia.And then the therapeutic effects of nimodipine were observed during ischemic and.reperfusion stages of the brain.It was found that BMg and BMg were decreased and CCaM HCaM increased during both the ischemic and reperfusion stages and BCa and MCo were increased during the reperfusion stage.The fact that calcium content was only increased during the reperfusion stage indicates that the influx of calcium plays an important role to precipitate injury during the reperfusion stage.Adminstration of nimodipine could prevent the increase of calcium and calmodulin and the decrease of magnesium after cerebral ischemia.
ABSTRACT
Male mice were subjected to 6 Gy total body irradiation,20% TBSA full thickness burns,or both the injuries respectively,and then lipid peroxides (LPO),vitamin E,sulfhydryl groups,respiratory control ratio (RCR),ADP/O ratio,and cytochrome oxidase activity of hepatic mitochondria were determined in the animals in the first 9 postinjury days.It was found that.1.LPO level increased in the early postinjury stage in the combined radiation-burn injury group.2.Vitamin E level decreased significantly in both the groups with either only irradiation or burns.3.The sulfhydryl groups showed a tendency to increase in all the 3 groups.4.The activity of cytochrome oxidase increased signficantly on the 7th postinjury day in the combined injury group.5.RCR and ADP/O ratios decreased more significantly in the combined injury group than in either the single injury group.These facts suggest that the suppression of the respiratory function of hepatic mitochondria results from the damage of mitochondrial membranes due to iipid peroxidation.
ABSTRACT
Objective To evaluate the effects of hydrogen peroxide (H 2O 2) on cardiomyocytes and the protective effect of pinacidil preconditioning on injured primary cultured cardiomyocytes. Methods We isolated and cultured cardiomyocytes in neonatal mice by trypsin digestion technique. The cells were inoculated in 96-well culture plate at the density of 1?10 5/ml. Cells were divided into control group and 400, 600, and 800 ?mol/L H 2O 2 treatment groups. MTT assay was used to determine the cell vitality at 1, 3, 6, 12, and 24 h after H 2O 2 treatment. The effects of pinacidil preconditioning were also observed. Results The effect of H 2O 2 on the damages to cardiomyocytes was in dose- and time-dependent manners. Pretreatment with pinacidil at the concentrations of 1?10 -4 , 1?10 -5 , and 1?10 -6 mol/L, particularly 1?10 -6 mol/L, could increase the activity of cardiomyocytes treated with H 2O 2. Conclusion Pinacidil preconditioning at lower doses can protected cardiomyocytes from injuries induced by H 2O 2.
ABSTRACT
Rats were divided into 3 groups and inflicted with total body irradiation of 5 Gy of gamma rays from a 60Co source,15% TBSA full thickness burns,or both of them respectively.The changes of lipid peroxide,cytochrome oxidase,NADH-cytochrome C reductase,catalase and superoxide dismutase activities were observed.It was found that the MDA content of hepatic mitochondria was significantly elevated in all the 3 goups on the 2nd and 6th day postinjury,and there was a third peak of MDA elevation in the the burn group on the 10th day postinjury.The increase of MDA in hepatic mitochondria was probably due the combined action of 2 factors.(1) increased production of toxic active oxygen species such as O2-and H2O2 as a result of increased activity of NADH-cytochrome C reductase and cytochrome oxidase,and (2) alterations of the defence mechanism against this active oxygen species due to lowered activity of superoxide dismutase and catalase.
ABSTRACT
The changes of skeletal muscle mitochondral monoamine oxidase (MAO) activity in rats fed with low Se grains from a Keshan-disease area were observed. The rats were killed at the time for feeding 30, 60 and 90 days respectiely. The mitochondrium of skeletal muscle was isolated MAO activity was determined with fluorescent methed. The results showed that in low-Se group the mitochondrial MAO activity was significantly decreased only at the time for 90 days feeding however GSH-px activity in red blood cells and Se content in plasma were significantly decreased at all experimental period as compared to Se-supplemented or stock died group.