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The article presents a study which investigates the toxicity level of pesticides to zebrafish (Brachydanio rerio). It states that the study used acute toxicity bioassays by exposing the fish to various concentrations of the test insecticides. The study concluded that there was very high toxicity levels of all pyrethroid insecticides and low toxicity level of organophosphate dichlorvos. It adds that the water quality requirement of the fish must be studied further.

Aim: To explore the effects of different doses of tyrosine modulation on behavioral performances in open field test of psychological stress rats., Methods: 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., Results: 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., Conclusion: 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.

Aim: To observe the impairment of homocysteine (Hcy) on neurons in vitro and the related mechanisms., Methods: 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., Results: 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., Conclusion: 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.

Objective: This study was conducted to evaluate the effects of different doses of zinc on the expression of metallothionein isoforms in hippocampus of stressed rats., Methods: The animal model of psychological stress was developed by restraint stress for four weeks. Wistar rats were randomly assigned to eight groups as follows: control group, zinc deficiency group, pair-feed group, zinc complementarity group and their corresponding stressed groups., Results: In zinc deficiency group, plasm zinc content was decreased, while in zinc complementarity group it's slightly increased. On the one hand, the expressions of metallothionein in brain and MT-1 mRNA, MT-3 mRNA in hippocampus were downregulated in zinc deficiency group, however, their expressions were evidently enhanced in stressed zinc deficiency group. On the other hand, inductions of metallothionein and it' s mRNAs in zinc complementarity group were increased, furthermore, stressed zinc complementarity group has more significantly yield of metallothionein and it' s mRNAs. In addition, the levels of plasma cortisol, IL-6, IL-1 and NO were increased clearly in zinc deficiency group and stressed zinc deficiency group., Conclusion: Our results suggested that zinc deficiency may decrease while zinc complementarity increase the expressions of metallothionein in brain and MT-1 mRNA, MT-3 mRNA in hippocampus, moreover, stress can increased their expressions dramatically. The impairment of stress on body may be involved with the nutrition status of zinc, and zinc deficiency can lower the body's resistibility to stress.

Objective: To study the influence of zinc deficiency on bone mineralization., Methods: 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., Results: 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., Conclusions: Zinc deficiency could lower the contents of parathyroid hormone and calcitonin in blood circulation affecting bone mineral deposit and causing defect in bone mineralization.