[Livestock and Poultry Faeces Nitrogen Loading Rate and Its Potential Return to Farmland in China].

To clearly analyze livestock and poultry faeces and the nitrogen loading rate of farmland in different provinces of China and their potential return to agricultural land, the changes of the output of various livestock and poultry faeces in China and the proportion of faeces from all types of livestock and poultry since 1978 were estimated in this paper based on statistical data and literature reviews using the pig manure equivalent (based on nitrogen) and the spatial distribution and pollution risk of livestock and the poultry faeces and nitrogen loading rates. Furthermore, the nitrogen return potential from animal faeces to farmland was analyzed and evaluated for different provinces of China in 2016. The results show that the pig manure equivalent (N) and total N from livestock and poultry faeces in China increases from 1978 to 2005 and is stable from 2005 to 2016. By 2016, the pig manure equivalent (N) and N were 366822.01×104 t and 2024.10×104 t, respectively, reflecting an increase by 105.78%. Approximately 94.03% to 98.34% of the faeces was from poultry, sheep, pigs, and cattle. The livestock and poultry faeces pig manure equivalent (N) and nutrient N were mainly distributed in North-Central China, especially in the Henan Province, accounting for 22.25% and 8.81% of the total in China, respectively, followed by the Sichuan Province. Based on the arable land, planting, and farmland areas, the pig faeces equivalent (N) and its N nutrient per unit area were calculated and the environmental risks were evaluated based on r values. Based on the arable land area, the southwestern and southeastern regions have large loading rates, while the northcentral region has a serious pollution risk of grade Ⅳ. Based on the planting area, the northwestern and southwestern regions have relatively large loading rates, while the northwestern and northcentral regions have pollution risks of grade Ⅲ. Based on the farmland area, the northcentral and southeastern regions have great loading rates and the northcentral region has a pollution risk of grade Ⅲ, Hunan has the largest loading rate, and Beijing, Shandong, and Henan have grade Ⅳ pollution risks. The livestock and poultry faeces pig manure equivalent (N) and amount of N nutrients returning to farmland in China are 113480.75×104 t and 626.15×104 t, respectively, equivalent to 3.07 t·hm-2 and 16.92 kg·hm-2, respectively, and the northcentral region has the largest rates with 8.27 t·hm-2 and 45.62 kg·hm-2, respectively. Based on 50% of the environmental capacity of faeces N, that is, 85 kg·hm-2, the N nutrient return can increase by 2520.21×104 t. The Heilongjiang Province has the greatest potential return, followed by the Sichuan Province.

Effects of epigallocatechin-3-gallate on behavioral impairments induced by psychological stress in rats.

This study was conducted to explore the effects of epigallocatechin-3-gallate (EGCG) on cognitive performances in psychological stress rats. An animal model of psychological stress was developed by restraint stress for three weeks. Male Wistar rats were randomly assigned to four groups as follows: normal control group, stress control group and two stress groups with green tea polyphenols (GTPs) and EGCG modulation, respectively. The changes of behavioral performances of rats were examined by the open-field test and step-through test. Results showed that behavioral performances of stress control group were changed abnormally, and they were improved in GTPs and EGCG modulation groups. In addition, plasma levels of cortisol, dopamine, norepinephrine, 5-hydroxytryptamine, interleukin-6 and interleukin-2 were detected. Stress control group had increased contents of cortisol, interleukin-6 and interleukin-2, and meanwhile had declined levels of 5-hydroxytryptamine and catecholamines. These changes in GTPs and EGCG modulation groups were similar to that of the normal control group. The expressions of metallothioneins in the hippocampus were detected by reverse transcription polymerase chain reaction. In contrast with the normal control group, their expressions in all the three stress groups were enhanced clearly. The results suggested that GTPs and EGCG modulation could improve the cognitive impairments induced by psychological stress. The related mechanisms may be involved with the changes of catecholamines, 5-hydroxytryptamine, cytokines and expressions of metallothioneins.

Protective effects of green tea polyphenols on cognitive impairments induced by psychological stress in rats.

This study was conducted to explore the modulation of GTPs on cognitive performances in psychological stress rats. Wistar rats were randomly assigned to five groups as follows: control group, stress group, and three stress groups with low, medium and high-doses of GTPs modulation respectively. The changes of cognitive performances were examined by open-field test, water maze and step-through test. Results demonstrated that serum levels of cortisol were all increased obviously in four stress groups. The cognitive performances of stress group were changed evidently. And these changes were improved in stress medium and high-doses of GTPs modulation groups. In addition, plasma levels of IL-6 and IL-2 were increased in four stress groups, serum norepinephrine and dopamine were decreased dramatically in stress group and stress low-dose GTPs modulation group. The serum norepinephrine and dopamine levels in stress medium and high-doses of GTPs modulation groups were increased in contrast to that of stress group. Furthermore, the changes of anti-oxidative capacity in brain tissue were also measured. Except superoxide dismutase, the changes of malondialdehyde, reactive oxidative species and total anti-oxidative capacity of stress group were significantly different from that of control group. These changes in stress medium and high-doses of GTPs modulation groups were improved. Our results suggested that psychological stress impaired body's cognitive performances, and moderate GTPs modulation could improve these abnormal changes. To our knowledge, this is the first report showing the improving effects of GTPs on cognitive dysfunctions induced by psychological stress.

[Effects of psychological stress on performances in open-field test of rats and tyrosine's modulation].

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.

[The impairment of homocysteine on neurons and the related mechanisms].

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.

Effects of zinc on the induction of metallothionein isoforms in hippocampus in stress rats.

Metallothioneins (MTs) are involved in the cellular metabolism of zinc and in cytoprotection against stress factors. Hippocampus plays a specific role in the body's response to stressors. The present study was conducted to evaluate the effects of zinc on the expression of metallothionein isoforms in the hippocampus of stress rats. The animal model of psychologic stress was developed by restraint for 4 weeks. Wistar rats were randomly assigned to 6 groups: control group, zinc-deficient group, zinc-supplemented group, and the corresponding 3 stress groups. Three separate diets of different zinc contents (1.73 ppm, 17.7 ppm, and 41.4 ppm, respectively) were used in this study. Compared with the control group, the stress groups had higher inductions of MTs and MT-1 and MT-3 mRNA in hippocampus. On the one hand, the expressions of MTs and their mRNAs in hippocampus were downregulated in the zinc-deficient group; however, their expressions were evidently enhanced in the stress zinc-deficient group. MT induction in the zinc-supplemented group was increased. Furthermore, the stress zinc-supplemented group had a more significant yield of MTs and their mRNAs. In addition, the levels of plasma cortisol, interleukin-6 (IL-6), IL-1, and nitric oxide (NO) were increased clearly in the zinc-deficient group and the stress groups. The results suggest that zinc deficiency may decrease and zinc supplementation may increase the expressions of MTs and their mRNAs in hippocampus; moreover, stress can increase their expressions dramatically. The impairment of stress on the body may be involved with the nutrition status of zinc, and zinc deficiency can lower the body's adaptability to stress.

[Effects of zinc on the expression of metallothionein isoforms in stressed hippocampal neurons in vitro].

AIM: To evaluate the effects of different doses of zinc on the expression of metallothionein isoforms in stressed hippocampal neurons in vitro. METHODS: The cell stress model was developed by corticosterone. The cultured hippocampal neurons were assigned to seven groups as follows: control group, zinc deficiency group, and their corresponding stressed groups, as well as three different levels of zinc complementarity groups. RESULTS: In zinc deficiency group, the expressions of metallothionein and MT-1 mRNA, MT-3 mRNA were downregulated. On the other hand, inductions of metallothionein and it's mRNAs in stressed zinc complementarity group were increased. In addition, the levels of supernatant IL-6 and NO were increased clearly in zinc deficiency group and corticosterone stressed groups. CONCLUSION: Our results suggest that zinc deficiency may decrease while zinc complementarity increase the expressions of metallothioneins and MT-1 mRNA, MT-3 mRNA in stressed hippocampal neurons in vitro.

[Effects of zinc on the expression of metallothionein isoforms in hippocampus of stressed rats].

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.

[Effect of zinc on the corticosterone-induced injury of primary cultured rat hippocampal neurons].

The effect of zinc on the damage of primary cultured hippocampal neurons induced by corticosterone (CORT) was studied. Neuronal injury and expression of NMDA receptor subunits (NR1,NR2A,NR2B) mRNA were detected by using in situ staining and RT-PCR, respectively. Neurons treated with 5 micromol/L CORT for 24 h showed decreased survival rates and increased apoptotic rates compared with the controls; co-application of CORT and 10 or 100 micromol/L Zn(2+) attenuated apoptotic rates while 250 micromol/L Zn(2+) worsened CORT-induced neuronal injury. Expression of NR1, NR2B mRNA in neurons treated by 5 micromol/L CORT for 24 h was significantly increased, while those concurrently added with 10 or 100 micromol/L Zn(2+) showed no changes. No statistic difference in NR2A mRNA was obtained under any treatment. These results suggest that zinc can bilaterally regulate neuronal injuries induced by CORT, among while NMDA receptors probably play an important role.

[Effects of zinc deficiency on bone mineralization and its mechanism in rats].

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.

[Effects of stress on hippocampal Glu-NMDAR pathway in rats and mechanism of zinc protection].

AIM: To observe the effects of stress on Glu uptake and NMDAR of hippocampus synaptosome in rats with different zinc status. METHODS: Stress model was established by photoelectric stimulus. The behaviors of rats were tested in open-field case. 3H-L-Glu was taken as radioligand to detect the NMDAR binding. Glu uptake was determined with radioimmunoassay. RESULTS: Compared with CT rats, ZD rats performed less movement in open-field test, both Bmax of NMDAR and 3H-L-Glu uptake of hippocampus in these rats were significantly decreased. Compared with corresponding non-stressed groups, the stressed groups appeared longer latency and less movement in open-field test. Increased Bmax of NMDAR and decreased 3H-L-Glu uptake were observed in all stressed rats, but only in SZD rats these indices showed statistical difference. CONCLUSION: Abnormal behaviors of rats induced by photoelectric stress were observed in open-field test, which was more serious in zinc deficiency rats. It is supposed that the Glu-NMDAR pathway is involved in the process of stress reaction. As it shows in our experiment, the changes of Bmax of NMDAR and 3H-L-Glu uptake of hippocampus synaptosome seems to be a part of the mechanisms of stress action.