Effects of seawater immersion on the functions of mitochondria of myocardium and hepatocyte in hemorrhagic shock rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of seawater immersion on the function of myocardium and hepatocyte mitochondria in experimental hemorrhagic shock rats.</p><p><b>METHODS</b>Twenty-four male Wistar rats were divided into three groups (n=8 in each group): control group, HSL group (hemorrhagic shock group on land) and HSS group (hemorrhagic shock group in seawater). The hemodynamic parameters, activities of H(+)-ATPase (adenosinetriphosphatase), succinate dehydrogenase (SDH) and Ca(2+)-Mg(2+)-ATPase, the calcium contents in myocardium and hepatocyte mitochondria were measured and the changes of proton translocation across the inner mitochondrial membrane were analyzed.</p><p><b>RESULTS</b>The hemodynamic indexes and the activities of H+-ATPase, SDH, Ca(2+)-Mg(2+)-ATPase in HSS group were significantly lower than those in control group and HSL group (P<0.05). In HSS group the calcium levels in tissue and mitochondria of myocardium and hepatocyte were elevated significantly compared with control group and HSL group (P<0.05). There was no significant difference in proton translocation among three groups.</p><p><b>CONCLUSIONS</b>This investigation demonstrates that seawater immersion can aggravate the conditions of hemorrhagic shock rats.</p>

Gene damages of mitochondrial DNA encoding cytochrome oxidase of intestinal epithelial cells in hemorrhagic shock rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells.</p><p><b>METHODS</b>Wistar rats were used and divided into two groups: hemorrhagic shock group and control group. Hemorrhagic shock model of rats was utilized in this experiment. The mtDNA was extracted from the intestinal epithelial cells and amplified by polymerase chain reaction (PCR) with different primers of cytochrome oxidase (COX I, COX II and COX III). The products of PCR were directly sequenced.</p><p><b>RESULTS</b>Hemorrhagic shock could result in the point mutagenesis in mitochondrial genome encoding cytochrome oxidase (COX I and COX II). There were 4, 4, 22, 16, 35 point mutations in COX I from 5545 to 6838 bp in 5 shocked rats. There were five point mutations in COX II from 7191 to 7542 bp at the site of t7191c, t7212c, a7386g, a7483g, c7542g in 1 shocked rat. There was no mutation found in COX III.</p><p><b>CONCLUSIONS</b>Hemorrhagic shock could significantly induce the damage of the gene of cytochrome oxidase encoded by mtDNA.</p>

Changes of proton transportation across the inner mitochondrial membrane and H(+)-ATPase in endotoxic shock rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the changes of proton transportation across the inner mitochondrial membrane (IMM) and H(+)-ATPase of hepatocytes in endotoxic shock rats.</p><p><b>METHODS</b>Endotoxin from E. Coil of 5.0 mg/kg or saline of 1 ml/kg was injected into the femoral vein. The rats were sacrificed pre-injection and 1, 3, 5, 8 hours after injection, and plasma and liver tissue samples were collected respectively. The liver tissue samples were used for preparation of mitochondria and submitochondrial particles (SMPs). The proton-translocation of SMPs and H(+)-ATPase, phospholipase A(2) (PLA(2)) activities and malondialdehyde (MDA) content, membrane fluidities of different level of mitochondria membrane and plasma MDA content were assayed.</p><p><b>RESULTS</b>(1) Five hours after E. Coli. O111B4 injection, the maximum fluorescence quenching ACMA after adding ATP, nicotinamide adenin dinucleoacid hydrogen (NADH), and the succinate were significantly decreased (P<0.05). The time of maximum fluorescent quenching and the half time of fluorescent quenching were significantly prolonged (P<0.01), especially when NADH was used as a substrate. (2) The mitochondrial H(+)-ATPase activity was significantly increased at early stage of endotoxic shock (P<0.05), and significantly decreased at late stage of endotoxic shock (P<0.01). (3) The mitochondrial membrane bound PLA(2) activity, plasmal and mitochondrial MDA content were significantly increased and succinate dehydrogenase (SDH) activity of mitochondria decreased markedly in endotoxic shock rats (P<0.05). (4) The mitochondrial membrane fluidity of different lipid regions was decreased, especially in the head of phospholipid.</p><p><b>CONCLUSIONS</b>Proton transportation across IMM and mitochondrial H(+)-ATPase activity are significantly decreased in endotoxic shock.</p>

Protective effect of serum containing Ziqi-liquid on hypoxia reoxygenation damaged intestinal epithelial cell 6 / 中华创伤杂志

Objective To observe the effect of hypoxia reoxygenation on activity of superoxide dismutase(SOD)and MDA content as well as[Ca~(2+)],concentration and mitochondria membrane poten- tial of intestinal epithelial cell-6(IEC-6)in IEC culture medium and explore the protective effect and mechanism of serum containing Ziqi-liquid(a preparation of Chinese herbal medicine)on hypoxia reoxy- genation damaged IEC-6.Methods Hypoxia reoxygenation damage model of IEC-6 was made.SOD activity and MPA content in IEC-6 culture medium were determined by ultraviolet spectrometry after hy- poxia reoxygenation and treatment with Ziqi-liquid.Meanwhile,MMP changes and[Ca~(2+)]concentration were detected by laser scanning confocal microscopy.Results After hypoxia reoxygenation,SOD and MMP were significantly decreased,but MDA content and[ Ca~(2+)] concentration significantly increased (P＜0.01),and significantly facilitated by serum containing Ziqi-liquid.Conclusion Hypoxia reoxy- genation can damage IEC-6,but the serum containing Ziqi-liquid has significant protective effect on it.