Effects of pyruvate on retinal oxidative damage and retinal ultrastructure in diabetic rats / 国际眼科杂志(Guoji Yanke Zazhi)

AlM:To investigate the changes of retinal histology and oxidative stress in diabetic retinopathy and its reversal by pyruvate in diabetic rats. METHODS: Eighty Wistar rats were divided into 3 groups:control group ( 20 rats ) , model group ( 30 rats ) and treatment group ( 30 rats ) . After streptozotocin ( STZ) induced diabetes mellitus in the model group and the treatment group, the treatment group received 2%pyruvate in diet and drinking. The changes of body weight and blood glucose were observed and the changes of glutathione peroxidase ( GSH-PX ) , malonie dialdehyde ( MDA) , and Na+-K+-ATPase levels of retinal tissue and retinal ultrastructure were investigated in three groups at 12wk after occurrence of diabetes. RESULTS: Compared with control group, the body weight of the model group were significantly decreased, the activities of GSH-PX and ATP in the retina of diabetic rats were significantly lower, the MDA was signigicantly higher and significant changes occurred in retinal ultrastructure. Compared with model group, the blood glucose of the treatment group had no significant changes. However, the activities of GSH and ATP in the retina of diabetic rats were higher, the MDA was lower and the retinal ultrastructure was comparatively mild. CONCLUSlON:Pyruvate can alleviate oxidatie stress reaction, improve the energy metabolism of retina, and delay the development of retinopathy.

Effects of psychological stress on performances in open-field test of rats and tyrosine's modulation / 中国应用生理学杂志

<p><b>AIM</b>To explore the effects of different doses of tyrosine modulation on behavioral performances in open field test of psychological stress rats.</p><p><b>METHODS</b>The animal model of psychological stress was developed by restraint stress for 21 days. Wistar rats were randomly assigned to five groups (n = 10) as follows: control group (CT), stress control group (SCT), low, medium and high-doses of tyrosine modulation stress groups (SLT, SMT and SIT). The changes of behavioral performances were examined by open-field test. Serum levels of cortisol, norepinephrine and dopamine were also detected.</p><p><b>RESULTS</b>The levels of serum cortisol were all increased obviously in the four stress groups, and their bodyweight gainings were diminished. The behavioral performances of SCT rats in open-field test were changed significantly in contrast to that of CT rats. However, The behavioral performances of SMT and SHT rats were not different from that of CT rats. In addition, the serum levels of norepinephrine and dopamine were downregulated obviously in SCT and SLT groups, and no differences were observed in other groups.</p><p><b>CONCLUSION</b>Psychological stress can impair body behavioral performances, and moderate tyrosine modulation may improve these abnormal changes. The related mechanisms may be involved with the changes of norepinephrine and dopamine.</p>

The impairment of homocysteine on neurons and the related mechanisms / 中国应用生理学杂志

<p><b>AIM</b>To observe the impairment of homocysteine (Hcy) on neurons in vitro and the related mechanisms.</p><p><b>METHODS</b>We examined the consequences of treatment of cultured rat cortical and hippocampal neurons with Hcy and detected the neurons' apoptosis, calcium influx, DNA damage and oxidative injury.</p><p><b>RESULTS</b>Primary cortical and hippocampal neurons were treated with Hcy (250 micromol/L) for 4 h resulted in apoptosis time-dependently. S-adenosyl methionine (SAM) could significantly, but MK-801, an NMDA receptor inhibitor, couldn't repress the Hcy induced neuron apoptosis. Hcy could induce neuron calcium overload through activating the NMDA receptors. The DNA of neurons was damaged by Hcy because the methylation reactions were inhibited. Hcy treatment also induced MDA level significantly increased, but did not affect the neurons' T-AOC.</p><p><b>CONCLUSION</b>These findings indicate that Hcy compromises neuronal homeostasis by multiple, divergent routes, including DNA damage, neuron exitotoxicity, and oxidative injury. Hcy mediated neuron apoptosis was mainly due to DNA damage.</p>

Effects of zinc deficiency on bone mineralization and its mechanism in rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the influence of zinc deficiency on bone mineralization.</p><p><b>METHODS</b>Thirty Wistar rats were randomly divided into three groups with ten in each group, i.e., zinc-deficient group (ZD), control group, and pair-fed group. Histomorphological changes of bone mineralization, bone mineral content and bone density, bone contents of zinc, calcium, phosphorus, magnesium, manganese, copper and hydroxyproline, and serum levels of parathyroid hormone, calcitonin and osteocalcin in the rats were measured.</p><p><b>RESULTS</b>The results showed that the mineral deposit rate and bone contents of zinc, phosphorus and hydroxyproline, and serum levels of calcitonin and osteocalcin lowered significantly in ZD group, as compared with those in the control and pair-fed groups, with (3.26 +/- 0.34) micro m/d, (64.54 +/- 2.34) g/kg, (54.4 +/- 9.5) mg/kg, (9.28 +/- 1.62) g/kg, (41.2 +/- 13.5) micro g/L, (82 +/- 30) micro g/L in ZD group; (5.37 +/- 0.53) micro m/d, (69.01 +/- 4.05) g/kg, (117.4 +/- 8.0) mg/kg, (11.31 +/- 1.30) g/kg, (68.3 +/- 14.4) micro g/L, (131 +/- 46) micro g/L in the control group; and (5.45 +/- 0.30) micro m/d, (67.81 +/- 3.56) g/kg, (106.7 +/- 8.4) mg/kg, (10.88 +/- 1.47) g/kg, (63.7 +/- 12.0) micro g/L, (120 +/- 52) micro g/L in the pair-fed group, respectively. While the time for mineralization lag and osteoid maturation obviously prolonged, (1.08 +/- 0.19) d and (7.12 +/- 2.30) d in ZD group, (0.39 +/- 0.06) d and (2.21 +/- 1.12) d in the control group, and (0.40 +/- 0.06) d and (2.12 +/- 0.58) d in the pair-fed group, respectively. In addition, bone mineral content and bone density and serum parathyroid hormone in ZD group decreased significantly and were lower than those in the control group, but not significantly different from those in the pair-fed group. There were no significant difference in femoral contents of calcium, magnesium, manganese and copper between the ZD group and the control and pair-fed groups.</p><p><b>CONCLUSIONS</b>Zinc deficiency could lower the contents of parathyroid hormone and calcitonin in blood circulation affecting bone mineral deposit and causing defect in bone mineralization.</p>