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61.
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63.
本文报道了用低能量He—Ne激光血管内照射治疗脑血栓形成35例,与常规药物治疗组30例对照,结果表明治疗组明显优于对照组(P<0.05),二者有显著性差异. 相似文献
64.
Magdalena J. Rossowska Parvaneh Ghanel Tetsuo Nakamoto 《Biological trace element research》1995,50(3):229-236
The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide
dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with
caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein
basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet);
or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake
of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and
Cu, Zn-superoxide dismutase (CUZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly
reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu, ZnSOD activity in the liver
of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities
in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of
antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were
lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects
of peroxides when compared to the liver. 相似文献
65.
We examined the effect of methionine deficiency on iodothyronine 5’-deiodinase activity in selenium-deficient rats or selenium-sufficient
rats fed sodium selenate or selenomethionine. Forty-two weanling male Wistar rats were divided into six groups and pair fed
the respective purifiedl-amino acid-based diets for 4 wk.l-methionine concentrations in the diet were 8.0 g/kg for sufficient rats, and 2.0 g/kg for deficient rats. Selenium concentrations
in the diet were 0.5 mg/kg (as sodium selenate or selenomethionine) for selenium-sufficient rats and less than 0.005 mg/kg
for selenium-deficient rats. Type I 5’-deiodinase activities were significantly lower in liver and higher in kidney of methionine-deficient
rats than in those of methionine-sufficient rats fed either the selenium-sufficient or the selenium-deficient diets. The type
I 5’-deiodinase activity in brain was significantly lower in the methionine-deficient rats than in the methionine-sufficient
rats fed the selenium-deficient diet. Type II 5’-deiodinase activity in brain was significantly higher in the methionine-deficient
rats than in the methionine-sufficient rats fed selenium-sufficient diet as sodium selenate. Both thyroxine and 3,3’,5-triiodothyronine
concentrations in plasma were significantly higher in the methionine-deficient rats than in the methionine-sufficient rats.
It is suggested that the methionine deficiency affects the 5’-deiodinase activity and thyroid hormones level in the rats. 相似文献
66.
Changes of Respiratory Chain Activity in Mitochondrial and Synaptosomal Fractions Isolated from the Gerbil Brain After Graded Ischaemia 总被引:4,自引:1,他引:3
Kathryn L. Allen Angeles Almeida Timothy E. Bates John B. Clark 《Journal of neurochemistry》1995,64(5):2222-2229
Abstract: In this study we have examined (1) the integrated function of the mitochondrial respiratory chain by polarographic measurements and (2) the activities of the respiratory chain complexes I, II–III, and IV as well as the ATP synthase (complex V) in free mitochondria and synaptosomes isolated from gerbil brain, after a 30-min period of graded cerebral ischaemia. These data have been correlated with cerebral blood flow (CBF) values as measured by the hydrogen clearance technique. Integrated functioning of the mitochondrial respiratory chain, using both NAD-linked and FAD-linked substrates, was initially affected at CBF values of ∼35 ml 100 g−1 min−1 , and declined further as the CBF was reduced. The individual mitochondrial respiratory chain complexes, however, showed differences in sensitivity to graded cerebral ischaemia. Complex I activities decreased sharply at blood flows below ∼30 ml 100 g−1 min−1 (mitochondria and synaptosomes) and complex II–III activities decreased at blood flows below 20 ml 100 g−1 min−1 (mitochondria) and 35–30 ml 100 g−1 min−1 (synaptosomes). Activities declined further as CBF was reduced below these levels. Complex V activity was significantly affected only when the blood flow was reduced below 15–10 ml 100 g−1 min−1 (mitochondria and synaptosomes). In contrast, complex IV activity was unaffected by graded cerebral ischaemia, even at very low CBF levels. 相似文献
67.
Abstract: Fetal alcohol syndrome produces defects that parallel abnormalities associated with early iron deficiency. Hence, we examined the effects of prenatal exposure to ethanol on iron, transferrin, and ferritin concentrations. The subjects were the offspring of pregnant rats fed an ethanol-containing diet (Et), pair-fed an isocaloric control diet (Ct), or fed chow and water. The amounts of iron, transferrin, and ferritin were assessed in three CNS regions (cerebral cortex, subcortical forebrain, and brain-stem). In all three segments of the control rats, iron, transferrin, and ferritin levels decreased during the first 2 postnatal weeks, reached a minimum during week 3, and then rose to adult levels. This pattern was delayed by ethanol treatment, e.g., the minimal concentrations in iron, transferrin, and ferritin in the Et-treated rats were achieved later (3 days, 7 days, and 2 weeks, respectively) than they were in the Ct-treated rats. Ethanol-induced alterations in iron homeostasis persisted into adulthood; iron concentration was reduced, transferrin concentration was unaffected, and ferritin concentration was increased. The net result was that the timely delivery and bioavailability of iron were compromised by ethanol exposure. The defects in iron regulation are permanent and may underlie ethanol-induced abnormalities in iron-dependent growth processes such as myelination. 相似文献
68.
Brain Quinolinic Acid in Chronic Experimental Hepatic Encephalopathy: Effects of an Exogenous Ammonium Acetate Challenge 总被引:1,自引:1,他引:0
Peter B. F. Bergqvist Melvyn P. Heyes †Mogens Bugge Finn Bengtsson 《Journal of neurochemistry》1995,65(5):2235-2240
Abstract: Elevated brain concentrations of the neurotoxin and NMDA receptor agonist quinolinic acid (QUIN) have been demonstrated in portacaval-shunted (PCS) rats, a chronic hepatic encephalopathy (HE) model. Increased brain QUIN levels have also been shown in acute hyperammonemic rats. In the present study, the plasma and brain (neocortical) QUIN levels in chronic PCS rats were investigated. The study also included a single exogenous ammonium acetate (NH4 Ac; 5.2 mmol/kg, i.p.) challenge to precipitate a reversible hepatic coma. Compared with sham-operated controls, chronic PCS rats exhibited decreased rather than increased plasma and brain QUIN levels. The plasma-to-brain QUIN ratio was not found to be altered. The NH4 Ac administration induced coma in all of the PCS rats 20–25 min after the challenge, and this coma was resolved within 60–75 min. No relevant temporal relationship between changes in brain QUIN levels and the neurological status in the PCS rats was observed. Therefore, our results do not support the contention that increased brain QUIN levels per se are involved in the pathogenesis of HE. 相似文献
69.
Seitaro Ohkuma Hidehiko Narihara Masashi Katsura Takeshi Hasegawa Kinya Kuriyama 《Journal of neurochemistry》1995,65(3):1109-1114
Abstract: The functional significance of peroxynitrite in the release of [3 H]GABA induced by nitric oxide (NO) liberated from NO generators was investigated using cerebral cortical neurons in primary culture. NO generators such as sodium nitroprusside (SNP) and S -nitroso- N -acetylpenicillamine (SNAP) increased [3 H]GABA release in a dose-dependent manner. These increases in [3 H]GABA release were significantly inhibited by hemoglobin, indicating that those NO generators evoke the release of [3 H]GABA by the formation of NO. Two types of superoxide scavengers, Cu2+ /Zn2+ superoxide dismutase and ceruloplasmin, significantly reduced the increase in [3 H]GABA release induced by both SNP and SNAP, which assumes that NO requires superoxide to induce [3 H]GABA release from the neurons. In addition, synthesized peroxynitrite induced a dose-dependent increase in [3 H]GABA release from the neurons. These results indicate that NO-induced [3 H]GABA release is mediated by peroxynitrite formed by the reaction of NO with superoxide. 相似文献
70.
Hideyuki Yamamoto Futosi Arakane Tsunehiko Ono Kazuhiro Tashima Eiichi Okumura Keisuke Yamada Shin-ichi Hisanaga Kohji Fukunaga Takeo Kishimoto Eishichi Miyamoto 《Journal of neurochemistry》1995,65(2):802-809
Abstract: Excitatory amino acid (EAA) neurotransmitters may play a role in the pathophysiology of traumatic injury to the CNS. Although NMDA receptor antagonists have been reported to have therapeutic efficacy in animal models of brain injury, these compounds may have unacceptable toxicity for clinical use. One alternative approach is to inhibit the release of EAAs following traumatic injury. The present study examined the effects of administration of a novel sodium channel blocker and EAA release inhibitor, BW1003C87, or the NMDA receptor-associated ion channel blocker magnesium chloride on cerebral edema formation following experimental brain injury in the rat. Animals (n = 33) were subjected to fluid percussion brain injury of moderate severity (2.3 atm) over the left parietal cortex. Fifteen minutes after injury, the animals received a constant infusion of BW1003C87 (10 mg/kg, i.v.), magnesium chloride (300 µmol/kg, i.v.), or saline over 15 min (2.75 ml/kg/15 min). In all animals, regional tissue water content in brain was assessed at 48 h after injury, using the wet weight/dry weight technique. In saline-treated control animals, fluid percussion brain injury produced significant regional brain edema in injured left parietal cortex ( p < 0.001), the cortical area adjacent to the site of maximal injury ( p < 0.001), left hippocampus ( p < 0.001), and left thalamus ( p = 0.02) at 48 h after brain injury. Administration of BW1003C87 15 min postinjury significantly reduced focal brain edema in the cortical area adjacent to the site of maximal injury ( p < 0.02) and left hippocampus ( p < 0.01), whereas magnesium chloride attenuated edema in left hippocampus ( p = 0.02). These results suggest that excitatory neurotransmission may play an important role in the pathogenesis of posttraumatic brain edema and that pre- or post-synaptic blockade of glutamate receptor systems may attenuate part of the deleterious sequelae of traumatic brain injury. 相似文献