ABSTRACT
[Objective] To discuss the effects of asphyxia on newborn baby ’s blood glucose, esp. the hypoglycemia. [Method] Choose 87 cases asphyxia newborn babies as observation group, compared with another 25 normal babies as control group, observe the relation between asphyxia degree and glucose concentration. [Result] In the observation group, the occurrence rates of hyperglycemia and hypoglycemia were much higher than control group, with dif-ference of statistical meaning. [Conclusion] The newborn babies of asphyxia are easy to have disordered glucose metabolism.
ABSTRACT
Objective To observe the effects of zinc-deficiency(ZD)on antioxidation system and repair of DNA damage and of hepatic cells by establishing an aging mice model induced with D-galactose. Methods Seventy 3-month-old male mice were divided randomly into 5 groups: normal young group, aging model group, aging+ZD group, aging+pair-fed group, aging+ZS group. The aging model were established with D-galactose (100mg/kg bw) by nap subcutaneous injection, while the young control group were injected with normal saline in the same way which lasted 30 days. Aging+ZD group and aging+ZS group were fed with ZD food(zinc 1.61?g/kg), others with normal food(zinc 50?g/kg). ZS food (zinc 100?g/kg)were given to aging+ZS group for the last 2 weeks in the course. On the 30 th day, all mice were killed by removing eyeballs and samples were collected immediately for later indexes detection. Results Compared with the aging control group, zinc contents and SOD activity of serum and liver decreased significantly, while MDA in the serum and liver and lipofuscin of liver increased much more in ZD mice. Comet assay also showed that the DNA damage of hepatic cells were more serious in aging ZD mice than in the control mice. The ratio of tail length/comet cell length in group ZD also increased significantly. However, moderate zinc supplement significantly improved all those indexes. Conclusions Zinc can affect the speed and degree of aging significantly. Zinc deficiency accelerates the aging progress; while moderate zinc supplement seems to be beneficial for retarding aging progress.
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Objective: To study the effects of zinc-deficiency(ZD)and zinc-supplement(ZS)on learning and memory in aging mice. Methods: Seventy 3-month-old male mice were divided randomly into 5 groups:normal young , aging model , aging+ZD, aging+pair-fed , aging+ZS . The aging model was established with D-galactose (100 mg/kg bw) by nape subcutaneous injection, while the young control group was injected with normal saline in the same way, which lasted 30 days. Aging+ZD and aging+ZS group were fed with ZD feed(zinc 1.61 mg/kg), others with normal feed(zinc 50 mg/kg). ZS feed(zinc 100 mg/kg)was given to aging+ZS for last 2 weeks. During the last week, the behavior tests were carried on. Finally the mice were all killed and samples were collected immediately for detection of indices . Results:Compared with the aging model group, ZD made serum zinc decrease significantly, the locomotor activity reduced and the ability of learning and memory weakened. Comet assay also showed that ZD induced DNA damage of cerebrum cells more serious in aging mice than the control. The ratio of tail length/comet cell length in Group ZD also increased significantly. However, moderate ZS could turn those indices better significantly. Conclusion: Zinc can ameliorate the learning and memory function of aging significantly. By reducing the function of DNA repair, ZD can act on learning and memory, while moderate ZS seems to be beneficial.
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Objective: To study the effect of vitamin A deficiency on lipid peroxidation and antioxidation system in rats. [WT5FZ]Methods: According to body weight, 33 Wistar male rats were randomly divided into 3 groups, A (Vitamin A complete deficiency group), B (Vitamin A low grade deficiency group), C (Vitamin A normal control group). The study lasted 84 days. The serum vitamin A, serum, liver and brain SOD activities, blood, liver and brain GSH Px activities, serum, liver and brain MDA were studied. Spin trapping techniques combined with ESR were used to capture and detect free radicals generated in liver. [WT5FZ]Results: In vitamin A completely deficient group and vitamin A low grade deficient group, SOD activities of serum, liver and brain, and the GSH Px activities of blood, liver and brain decreased significantly, while LPO contents of serum, liver and serum increased markedly, and typical free radicals peaks in liver were indicated by ESR spectra. [WT5FZ]Conclusion: Vitamin A deficiency results in decrease of antioxidation capacity and increase of lipid peroxidation.