1999年7月美国临床生化研究院（National Academy of Clinical Biochemistry．NACB）发表了检验医学实践指南（Laboratory Medicine Practice Guidelines，LMPG）：关于在冠状动脉疾病时心肌标志物的使用。自从这个初始文件发表8年以来...1999年7月美国临床生化研究院（National Academy of Clinical Biochemistry．NACB）发表了检验医学实践指南（Laboratory Medicine Practice Guidelines，LMPG）：关于在冠状动脉疾病时心肌标志物的使用。自从这个初始文件发表8年以来，在世界范围内对心肌损伤生化标志物的认识和应用有了很大的进展．实际上已扩展了生化标志物利用的推荐范围。有鉴于此，NACB指令LMPG委员会负责修订和扩展早期的推荐，以建立适应现代的指南。展开更多
Plant volatiles induced by wounding play key roles in plant-insect and plant-plant interactions. To deeply understand the mechanism of their induction by wounding and their functions in interplant communications, four...Plant volatiles induced by wounding play key roles in plant-insect and plant-plant interactions. To deeply understand the mechanism of their induction by wounding and their functions in interplant communications, four diverse tree species: ashleaf maples ( Acer negundo L.), hankow willow (Salix matsudana Koidz.), Chinese white poplar ( Populus tomentosa Carr.) and poplar opera 8277 (P. simonii x P. pyramibalis cv.), were used as materials. The blends of volatiles collected after damage were detected with GCMS. Most of the induced compounds reach high concentrations in 5 h. They are acyclic monoterpenes, fatty acid derivatives, and aromatic compounds. To authors' knowledge, dimethyl adipate, diisobutyl succinate and benthothiazole have never been reported in previous herbivore insect-plant systems, After being damaged 2 h, green leaf volatiles were released in large amount. The repellents were detected in higher concentration after 24 h. The time of releasing is different within different species, but many kinds of volatiles widely existed in different trees. There were some difference among species. Health ashleaf maple released more terpenoids, but poplars and willow produced more aromatic compounds.展开更多
Drug-induced liver injury is a significant and still unresolved clinical problem. Limitations to knowledge about the mechanisms of toxicity render incomplete the detection of hepatotoxic potential during preclinical d...Drug-induced liver injury is a significant and still unresolved clinical problem. Limitations to knowledge about the mechanisms of toxicity render incomplete the detection of hepatotoxic potential during preclinical development. Several xenobiotics are lipophilic substances and their transformation into hydrophilic compounds by the cytochrome P-450 system results in production of toxic metabolites. Aging, preexisting liver disease, enzyme induction or inhibition, genetic variances, local 02 supply and, above all, the intrinsic molecular properties of the drug may affect this process. Necrotic death follows antioxidant consumption and oxidation of intracellular proteins, which determine increased permeability of mitochondrial membranes, loss of potential, decreased ATP synthesis, inhibition of Ca^2＋-dependent ATPase, reduced capability to sequester Ca^2＋ within mitochondria, and membrane bleb formation. Conversely, activation of nucleases and energetic participation of mitochondria are the main intracellular mechanisms that lead to apoptosis. Non-parenchymal hepatic cells are inducers of hepatocellular injury and targets for damage. Activation of the immune system promotes idiosyncratic reactions that result in hepatic necrosis or cholestasis, in which different HLA genotypes might play a major role. This review focuses on current knowledge of the mechanisms of drug-induced liver injury and recent advances on newly discovered mechanisms of liver damage. Future perspectives including new frontiers for research are discussed.展开更多
AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided...AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups (groups 1-5). During the experiment, animals of Group 1 drank only water. The other four groups (2-5) drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin and bilirubin were measured colorimetrically. Lipid peroxidation (thiobarbituric-acid reactive substances, TBARS) both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS: Compared with sham group, serum AST and ALT increased significantly under ethanol treatment (43% and 93%, respectively, with P < 0.05). Vitamin C and vitamin E treatment attenuated the ethanol-induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group (3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P < 0.05). During liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation (4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P < 0.05). In association with hepatic injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins (C and E) treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION: Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.展开更多
The attenuating effect of daidzein (DAI) on oxidative toxicity induced by Aroclor 1254 (A1254) was investigated in mouse testicular cells. Cells were exposed to A1254 alone or with DAI. The oxidative damage was estima...The attenuating effect of daidzein (DAI) on oxidative toxicity induced by Aroclor 1254 (A1254) was investigated in mouse testicular cells. Cells were exposed to A1254 alone or with DAI. The oxidative damage was estimated by measuring malondialdehyde (MDA) formation, superoxide dismutase (SOD) activity and glutathione (GSH) content. Results show that A1254 induced a decrease of germ cell number, an elevation in thiobarbituric acid reactive substances (TBARS) but a decrease in SOD activity and GSH content. However, simultaneous supplementation with DAI decreased TBARS level and increased SOD activity and GSH content. Consequently, dietary DAI may restore the intracellular antioxidant system to attenuate the oxidative toxicity of A1254 in testicular cells.展开更多
AIM： TO investigate the dynamic change and role of neuronal nitric oxide synthase （nNOS） and inducible nitric oxide synthase （iNOS） in neonatal rat with intestinal injury and to define whether necrotizing enteroc...AIM： TO investigate the dynamic change and role of neuronal nitric oxide synthase （nNOS） and inducible nitric oxide synthase （iNOS） in neonatal rat with intestinal injury and to define whether necrotizing enterocolitis （NEC） is associated with the levels of nitric oxide synthase （NOS） in the mucosa of the affected intestine tissue. METHODS： Wistar rats less than 24 h in age received an intraperitoneal injection with 5 mg/kg lipopolysaccharide （LPS）. Ileum tissues were collected at 1, 3, 6, 12 and 24 h following LPS challenge for histological evaluation of NEC and for measurements of nNOS and iNOS. The correlation between the degree of intestinal injury and levels of NOS was determined. RESULTS： The LPS-injected increase in injury scores pups showed a significant versus the control. The expression of nNOS protein and mRNA was diminished after LPS injection. There was a negative significant correlation between the nNOS protein and the grade of median intestinal injury within 24 h. The expression of iNOS protein and mRNA was significantly increased in the peak of intestinal injury. CONCLUSION： nNOS and iNOS play different roles in LPS-induced intestinal injury. Caution should be exerted concerning potential therapeutic uses of NOS inhibitors in NEC.展开更多
AIM;Oxidative stress participates in the cell carcinogenesis by inducing DNA mutations.Our aim was to assess whether ascorbic acid,an antioxidant,could have a role in preventing ROS(Reactive Oxygen Species)generation ...AIM;Oxidative stress participates in the cell carcinogenesis by inducing DNA mutations.Our aim was to assess whether ascorbic acid,an antioxidant,could have a role in preventing ROS(Reactive Oxygen Species)generation in experimental gastric carcinoma in a rat model. METHODS:Experimental gastric cancer was induced in twelve Wistar male rats(weighting 250-350 g)by profound duodeno-gastric reflux throught split gastrojenunostomy.The rats were allocated to the following groups:Group Ⅰ(n=6) was the control;Group Ⅱ(n=6)which was mantained with daily intake of tape water with Vitamin C(30 mg/Kg).After 6 or 12 months,samples of gastric tumor or non tumor mucosa were taken from the anastomosis of both groups. Oxidative stress was measured by superoxide quantification through lucigenin-amplified chemiluminescence base and by staining with Nitrobluetetrazolium.The histopathologic confirmation of adenocarcinoma was made by eosin- hemathoxilin method. RESULTS:The intestinal type of gastric adenocarcinoma was microscopically identified in all animals of group Ⅰ whereas only 3 rats of group Ⅱ showed an adenocarcinoma without macroscopic evidence of them.The cancers were located in the anastomosis in all cases.Basal luminescence from tumor gastric tissue generated 38.4±6.8 count per minute/mg/×10~6(mean±SD)and 14.9±4.0 count per minute/mg/×10~6,respectively,in group Ⅰ and Ⅱ animals(P <0.05).The Nitrobluetetrazolium method showed intense staining in tumor tissues but not in non neoplasic mucosa. CONCLUSION:Experimental gastric tumors seem to produce more reactive oxygen species than non neoplasic gastric tissue.The reduction of oxidative stress and gastric tumor incidence in rats were induced by the intake of ascorbic acid.Therefore,it may have a role in the prevention of gastric carcinoma. Oliveira CPMS Kassab P Lopasso FP Souza HP Janiszewski M Laurindo FRM Iriya K Laudanna AA.Protective effect of ascorbic acid in experimental gastric cancer:reduction of oxidative stress.World J Gastroenterol 2003;9(3):446-448 http://www.wjgnet.com/1007-9327/9/446.htm展开更多
The hepatocyte, the main cellular component of the liver, exhibits variable susceptibility to different types of injury induced by endogenous or exogenous factors. Hepatocellular dysfunction or death and regeneration ...The hepatocyte, the main cellular component of the liver, exhibits variable susceptibility to different types of injury induced by endogenous or exogenous factors. Hepatocellular dysfunction or death and regeneration are dependent upon the complicated interactions between numerous biologically active molecules. Platelet- activating factor （PAF） seems to play a pivotal role as the key mediator of liver injury in the clinical and experimental setting, as implied by the beneficial effects of its receptor antagonists. A comprehensive up-to-date overview of the specific functional and regulatory properties of PAF in conditions associated with liver injury is attempted in this review.展开更多
文摘1999年7月美国临床生化研究院（National Academy of Clinical Biochemistry．NACB）发表了检验医学实践指南（Laboratory Medicine Practice Guidelines，LMPG）：关于在冠状动脉疾病时心肌标志物的使用。自从这个初始文件发表8年以来，在世界范围内对心肌损伤生化标志物的认识和应用有了很大的进展．实际上已扩展了生化标志物利用的推荐范围。有鉴于此，NACB指令LMPG委员会负责修订和扩展早期的推荐，以建立适应现代的指南。
文摘Plant volatiles induced by wounding play key roles in plant-insect and plant-plant interactions. To deeply understand the mechanism of their induction by wounding and their functions in interplant communications, four diverse tree species: ashleaf maples ( Acer negundo L.), hankow willow (Salix matsudana Koidz.), Chinese white poplar ( Populus tomentosa Carr.) and poplar opera 8277 (P. simonii x P. pyramibalis cv.), were used as materials. The blends of volatiles collected after damage were detected with GCMS. Most of the induced compounds reach high concentrations in 5 h. They are acyclic monoterpenes, fatty acid derivatives, and aromatic compounds. To authors' knowledge, dimethyl adipate, diisobutyl succinate and benthothiazole have never been reported in previous herbivore insect-plant systems, After being damaged 2 h, green leaf volatiles were released in large amount. The repellents were detected in higher concentration after 24 h. The time of releasing is different within different species, but many kinds of volatiles widely existed in different trees. There were some difference among species. Health ashleaf maple released more terpenoids, but poplars and willow produced more aromatic compounds.
文摘Drug-induced liver injury is a significant and still unresolved clinical problem. Limitations to knowledge about the mechanisms of toxicity render incomplete the detection of hepatotoxic potential during preclinical development. Several xenobiotics are lipophilic substances and their transformation into hydrophilic compounds by the cytochrome P-450 system results in production of toxic metabolites. Aging, preexisting liver disease, enzyme induction or inhibition, genetic variances, local 02 supply and, above all, the intrinsic molecular properties of the drug may affect this process. Necrotic death follows antioxidant consumption and oxidation of intracellular proteins, which determine increased permeability of mitochondrial membranes, loss of potential, decreased ATP synthesis, inhibition of Ca^2＋-dependent ATPase, reduced capability to sequester Ca^2＋ within mitochondria, and membrane bleb formation. Conversely, activation of nucleases and energetic participation of mitochondria are the main intracellular mechanisms that lead to apoptosis. Non-parenchymal hepatic cells are inducers of hepatocellular injury and targets for damage. Activation of the immune system promotes idiosyncratic reactions that result in hepatic necrosis or cholestasis, in which different HLA genotypes might play a major role. This review focuses on current knowledge of the mechanisms of drug-induced liver injury and recent advances on newly discovered mechanisms of liver damage. Future perspectives including new frontiers for research are discussed.
文摘AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups (groups 1-5). During the experiment, animals of Group 1 drank only water. The other four groups (2-5) drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin and bilirubin were measured colorimetrically. Lipid peroxidation (thiobarbituric-acid reactive substances, TBARS) both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS: Compared with sham group, serum AST and ALT increased significantly under ethanol treatment (43% and 93%, respectively, with P < 0.05). Vitamin C and vitamin E treatment attenuated the ethanol-induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group (3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P < 0.05). During liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation (4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P < 0.05). In association with hepatic injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins (C and E) treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION: Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.
基金the Program for New Century Excellent Talentsin University of the Ministry of Education of China (No. NCET-05-0514)the Postdoctoral Science Foundation of China (No. 20060400325)
文摘The attenuating effect of daidzein (DAI) on oxidative toxicity induced by Aroclor 1254 (A1254) was investigated in mouse testicular cells. Cells were exposed to A1254 alone or with DAI. The oxidative damage was estimated by measuring malondialdehyde (MDA) formation, superoxide dismutase (SOD) activity and glutathione (GSH) content. Results show that A1254 induced a decrease of germ cell number, an elevation in thiobarbituric acid reactive substances (TBARS) but a decrease in SOD activity and GSH content. However, simultaneous supplementation with DAI decreased TBARS level and increased SOD activity and GSH content. Consequently, dietary DAI may restore the intracellular antioxidant system to attenuate the oxidative toxicity of A1254 in testicular cells.
文摘AIM： TO investigate the dynamic change and role of neuronal nitric oxide synthase （nNOS） and inducible nitric oxide synthase （iNOS） in neonatal rat with intestinal injury and to define whether necrotizing enterocolitis （NEC） is associated with the levels of nitric oxide synthase （NOS） in the mucosa of the affected intestine tissue. METHODS： Wistar rats less than 24 h in age received an intraperitoneal injection with 5 mg/kg lipopolysaccharide （LPS）. Ileum tissues were collected at 1, 3, 6, 12 and 24 h following LPS challenge for histological evaluation of NEC and for measurements of nNOS and iNOS. The correlation between the degree of intestinal injury and levels of NOS was determined. RESULTS： The LPS-injected increase in injury scores pups showed a significant versus the control. The expression of nNOS protein and mRNA was diminished after LPS injection. There was a negative significant correlation between the nNOS protein and the grade of median intestinal injury within 24 h. The expression of iNOS protein and mRNA was significantly increased in the peak of intestinal injury. CONCLUSION： nNOS and iNOS play different roles in LPS-induced intestinal injury. Caution should be exerted concerning potential therapeutic uses of NOS inhibitors in NEC.
文摘AIM;Oxidative stress participates in the cell carcinogenesis by inducing DNA mutations.Our aim was to assess whether ascorbic acid,an antioxidant,could have a role in preventing ROS(Reactive Oxygen Species)generation in experimental gastric carcinoma in a rat model. METHODS:Experimental gastric cancer was induced in twelve Wistar male rats(weighting 250-350 g)by profound duodeno-gastric reflux throught split gastrojenunostomy.The rats were allocated to the following groups:Group Ⅰ(n=6) was the control;Group Ⅱ(n=6)which was mantained with daily intake of tape water with Vitamin C(30 mg/Kg).After 6 or 12 months,samples of gastric tumor or non tumor mucosa were taken from the anastomosis of both groups. Oxidative stress was measured by superoxide quantification through lucigenin-amplified chemiluminescence base and by staining with Nitrobluetetrazolium.The histopathologic confirmation of adenocarcinoma was made by eosin- hemathoxilin method. RESULTS:The intestinal type of gastric adenocarcinoma was microscopically identified in all animals of group Ⅰ whereas only 3 rats of group Ⅱ showed an adenocarcinoma without macroscopic evidence of them.The cancers were located in the anastomosis in all cases.Basal luminescence from tumor gastric tissue generated 38.4±6.8 count per minute/mg/×10~6(mean±SD)and 14.9±4.0 count per minute/mg/×10~6,respectively,in group Ⅰ and Ⅱ animals(P <0.05).The Nitrobluetetrazolium method showed intense staining in tumor tissues but not in non neoplasic mucosa. CONCLUSION:Experimental gastric tumors seem to produce more reactive oxygen species than non neoplasic gastric tissue.The reduction of oxidative stress and gastric tumor incidence in rats were induced by the intake of ascorbic acid.Therefore,it may have a role in the prevention of gastric carcinoma. Oliveira CPMS Kassab P Lopasso FP Souza HP Janiszewski M Laurindo FRM Iriya K Laudanna AA.Protective effect of ascorbic acid in experimental gastric cancer:reduction of oxidative stress.World J Gastroenterol 2003;9(3):446-448 http://www.wjgnet.com/1007-9327/9/446.htm
文摘The hepatocyte, the main cellular component of the liver, exhibits variable susceptibility to different types of injury induced by endogenous or exogenous factors. Hepatocellular dysfunction or death and regeneration are dependent upon the complicated interactions between numerous biologically active molecules. Platelet- activating factor （PAF） seems to play a pivotal role as the key mediator of liver injury in the clinical and experimental setting, as implied by the beneficial effects of its receptor antagonists. A comprehensive up-to-date overview of the specific functional and regulatory properties of PAF in conditions associated with liver injury is attempted in this review.
