Zinc transporter expression profiles in the rat prostate following alterations in dietary zinc

Zinc plays important roles in numerous cellular activities and physiological functions. Intracellular zinc levels are strictly maintained by zinc homeostatic mechanisms. Zinc concentrations in the prostate are the highest of all soft tissues and could be important for prostate health. However, the mechanisms by which the prostate maintains high zinc levels are still unclear. In addition, the response of the prostate to alterations in dietary zinc is unknown. The current study explored cellular zinc levels and zinc transporter expression profiles in the lobes of the prostate during dietary marginal zinc depletion. Rats were given either zinc-adequate (ZA, 30 mg Zn/kg) or marginal zinc-deficient (MZD, 5 mg Zn/kg) diet for 9 weeks. In addition, a subgroup of the MZD rats was supplemented with phytase (1,500 unit/kg diet) to improve zinc bioavailability. We found that both zinc concentrations and ZnT2 expression in the prostate dorsolateral lobes were substantially higher than in the ventral lobes (P < 0.05). Marginal zinc depletion significantly decreased ZnT2 expression in the dorsolateral lobes (P < 0.05), and phytase supplementation had a trend to increase ZnT2 expression. In addition, of all measured zinc transporters, only ZnT2 mRNA abundance was significantly correlated to the zinc concentrations in the dorsolateral lobe. No correlations were found between zinc transporter expression and zinc concentrations in the ventral lobes. These results indicate that ZnT2 may play a significant role in the maintenance of zinc homeostasis in the prostate.     

Dietary Fiber Intake Increases the Risk of Zinc Deficiency in Healthy and Diabetic Women

Phytic acid is a major determinant of zinc bioavailability. Little is known about phytic acid intakes or indices of zinc bioavailability in type 2 diabetes mellitus (DM), a condition that predisposes to zinc deficiency. The aim of this cross-sectional study was to measure and explore the relationships among phytic acid intake, zinc bioavailability, and molecular markers of zinc homeostasis in 20 women with DM compared to 20 healthy women. The phytate/zinc, (calcium)(phytate)/zinc, and (calcium + magnesium)(phytate)/zinc molar ratios were used to indicate zinc bioavailability. Plasma zinc concentrations and zinc transporter (ZnT1, ZnT8, and Zip1) gene expression in mononuclear cells were measured. Participants with DM consumed 1,194?±?824?mg/day (mean?±?SD) phytic acid, an amount similar to the intake of healthy women (1,316?±?708?mg/day). Bread products and breakfast cereals contributed more than 40?% of the phytic acid intake in each group. A positive relationship was observed in all participants between phytic acid and dietary fiber (r?=?0.6, P?<?0.001) and between dietary fiber and the (calcium)(phytate)/zinc ratio (r?=?0.5, P?<?0.001). Compared to the healthy group, the messenger RNA ratio of ZnT1 (zinc export) to Zip1 (zinc import) was lower in participants with DM, which may indicate perturbed zinc homeostasis in the disorder. The plasma zinc concentration was not predicted by age, body mass index, health status, zinc bioavailability, or zinc transporter expression. Healthy and diabetic women consume phytic acid in amounts that are likely to decrease the bioavailability of dietary zinc. Recommendations to consume greater amounts of dietary fiber, much of which is associated with phytate, increase the risk of zinc deficiency.     

脊髓缺血损伤合并脓毒症后脊髓ZnT1表达的研究

目的：研究脊髓缺血损伤合并脓毒血症后大鼠脊髓的病理改变及脊髓组织中锌转运体1（zinc transporter1,ZnT1）的表达规律。方法：将32只wistar大鼠随机分为假手术组（s组,n=8）、腹主动脉阻断组（I／R组,n=8）、内毒素组（LPS组,n=8）和腹主动脉阻断＋内毒素组（I／R＋LPS组,n=8）。用HE染色的方法检测脊髓组织病理损害,用免疫组织化学的方法检测脊髓组织中ZnTl的表达规律。结果：1．病理结果改变：除S组外,I／R组、LPS组、UR＋LPS组三组大鼠HE染色切片中均可见脊髓组织损伤,各组脊髓损伤的严重程度有以下规律：S组〈I/R组〈LPS组〈I／R＋LPS组。2．免疫组化结果：脊髓损伤组ZnT1的表达较假手术组均增加（P〈0．05）。结论：1．脊髓缺血损伤合并内毒素攻击可导致严重的脊髓损伤。2．腹主动脉阻断合并内毒素攻击所致脊髓损伤早期脊髓组织中ZnT1表达上调,可能通过调节脊髓损伤早期脊髓组织中锌稳态平衡进而在脊髓损伤后脊髓神经元的病理生理活动中发挥重要作用,这一实验结果可为寻找早期脊髓损伤预防措施提供新的思路。     

Astaxanthin Modulates Autophagy,Apoptosis, and Neuronal Oxidative Stress in a Rat Model of Compression Spinal Cord Injury

The effects of astaxanthin (AST) were evaluated on oxidative mediators, neuronal apoptosis, and autophagy in functional motor recovery after spinal cord injury (SCI). Rats were divided into three groups of sham, SCI?+?DMSO (dimethyl sulfoxide), and SCI?+?AST. Rats in the sham group only underwent a laminectomy at thoracic 8–9. While, the SCI?+?DMSO and SCI?+?AST groups had a compression SCI with an aneurysm clip. Then, this groups received an intrathecal (i.t.) injection of 5% DMSO and AST (10 μl of 0.005 mg/kg), respectively. The rat motor functions were assessed weekly until the 28th day using a combined behavioral score (CBS). Total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were measured in spinal tissue to evaluate oxidative stress-related parameters. Besides, autophagy-related proteins (P62, LC3B, and Beclin1) and apoptosis-associated proteins (Bax and Bcl2) were determined using western blotting on the 1st and 7th days after surgery. Hematoxylin–eosin and Fluoro-Jade B staining were performed to detect the histological alterations and neuronal degeneration. As the result, treatment with AST potentially attenuated rat CBS scores (p?<?0.001) towards a better motor performance. AST significantly reduced the spinal level of oxidative stress by increasing TAC, SOD, and GPx, while decreasing MDA (p?<?0.001). Furthermore, AST treatment remarkably upregulated expression of LC3B (p?<?0.001), and Beclin1 (p?<?0.05) in the spinal cord, but downregulated P62 (p?<?0.05) and the Bax/Bcl2 ratio (p?<?0.001). Consequently, AST reduced SCI-induced histological alterations and neuronal degeneration (p?<?0.001). In conclusion, AST can improve motor function after SCI by reducing oxidative stress/apoptosis and increasing neuronal autophagy.

     

Spatiotemporal Patterns of SSeCKS Expression After Rat Spinal Cord Injury

Src suppressed C kinase substrate (SSeCKS) was identified as a PKC substrate/PKC-binding protein, which plays a role in mitogenic regulatory activity and has a function in the control of cell signaling and cytoskeletal arrangement. However its distribution and function in the central nervous system (CNS) lesion remain unclear. In this study, we mainly investigated the mRNA and protein expression and cellular localization of SSeCKS during spinal cord injury (SCI). Real-time PCR and Western blot analysis revealed that SSeCKS was present in normal whole spinal cord. It gradually increased, reached a peak at 3 days for its mRNA level and 5 days for its protein level after SCI, and then declined during the following days. In ventral horn, the expression of SSeCKS underwent a temporal pattern that was similar with the whole spinal cord in both mRNA and protein level. However, in dorsal horn, the mRNA and protein for SSeCKS expression were significantly increased at 1 day for its mRNA level and 3 days for its protein level, and then gradually declined to the baseline level, ultimately up-regulated again from 7 to 14 days. The protein expression of SSeCKS was further analysed by immunohistochemistry. The positively stained areas for SSeCKS changed with the similar pattern to that of protein expression detected by immunoblotting analysis. Double immunofluorescence staining showed that SSeCKS immunoreactivity (IR) was found in neurons, astrocytes, oligodendrocytes of spinal cord tissues within 5 mm from the lesion site. Importantly, injury-induced expression of SSeCKS was co-labeled by active caspase-3 (apoptotic marker), Tau-1 (the marker for pathological oligodendrocyte) and β-1,4-galactosyltransferase 1 (GalT). All the results suggested that SSeCKS might play important roles in spinal cord pathophysiology and further research is needed to have a good understanding of its function and mechanism. Feng Xiao and Min Fei contributed equally to this work.     

Persistent At-Level Thermal Hyperalgesia and Tactile Allodynia Accompany Chronic Neuronal and Astrocyte Activation in Superficial Dorsal Horn following Mouse Cervical Contusion Spinal Cord Injury

In humans, sensory abnormalities, including neuropathic pain, often result from traumatic spinal cord injury (SCI). SCI can induce cellular changes in the CNS, termed central sensitization, that alter excitability of spinal cord neurons, including those in the dorsal horn involved in pain transmission. Persistently elevated levels of neuronal activity, glial activation, and glutamatergic transmission are thought to contribute to the hyperexcitability of these dorsal horn neurons, which can lead to maladaptive circuitry, aberrant pain processing and, ultimately, chronic neuropathic pain. Here we present a mouse model of SCI-induced neuropathic pain that exhibits a persistent pain phenotype accompanied by chronic neuronal hyperexcitability and glial activation in the spinal cord dorsal horn. We generated a unilateral cervical contusion injury at the C5 or C6 level of the adult mouse spinal cord. Following injury, an increase in the number of neurons expressing ΔFosB (a marker of chronic neuronal activation), persistent astrocyte activation and proliferation (as measured by GFAP and Ki67 expression), and a decrease in the expression of the astrocyte glutamate transporter GLT1 are observed in the ipsilateral superficial dorsal horn of cervical spinal cord. These changes have previously been associated with neuronal hyperexcitability and may contribute to altered pain transmission and chronic neuropathic pain. In our model, they are accompanied by robust at-level hyperaglesia in the ipsilateral forepaw and allodynia in both forepaws that are evident within two weeks following injury and persist for at least six weeks. Furthermore, the pain phenotype occurs in the absence of alterations in forelimb grip strength, suggesting that it represents sensory and not motor abnormalities. Given the importance of transgenic mouse technology, this clinically-relevant model provides a resource that can be used to study the molecular mechanisms contributing to neuropathic pain following SCI and to identify potential therapeutic targets for the treatment of chronic pathological pain.     

Effects of Zinc Glycinate on Productive and Reproductive Performance,Zinc Concentration and Antioxidant Status in Broiler Breeders

An experiment was conducted to investigate the effects of zinc glycinate (Zn-Gly) supplementation as an alternative for zinc sulphate (ZnSO₄) on productive and reproductive performance, zinc (Zn) concentration and antioxidant status in broiler breeders. Six hundred 39-week-old Lingnan Yellow broiler breeders were randomly assigned to 6 groups consisting of 4 replicates with 25 birds each. Breeders were fed a basal diet (control group, 24 mg Zn/kg diet), basal diet supplemented with 80 mg Zn/kg diet from ZnSO₄ or basal diet supplemented with 20, 40, 60 and 80 mg Zn/kg diet from Zn-Gly. The experiment lasted for 8 weeks after a 4-week pre-test with the basal diet, respectively. Results showed that Zn supplementation, regardless of sources, improved (P?<?0.05) the feed conversion ratio (kilogram of feed/kilogram of egg) and decreased broken egg rate, and elevated (P?<?0.05) the qualified chick rate. Compared with the ZnSO₄ group, the 80 mg Zn/kg Zn-Gly group significantly increased (P?<?0.05) average egg weight, fertility, hatchability and qualified chick rate, whereas it decreased (P?<?0.05) broken egg rate. The Zn concentrations in liver and muscle were significantly higher (P?<?0.05) in 80 mg Zn/kg Zn-Gly group than that in ZnSO₄ group. Compared with ZnSO₄ group, 80 mg Zn/kg Zn-Gly group significantly elevated (P?<?0.05) the mRNA abundances of metallothionein (MT) and copper-zinc superoxide (Cu-Zn SOD), as well as the Cu-Zn SOD activity and MT concentration in liver. Moreover, the 80 mg Zn/kg Zn-Gly group had higher (P?<?0.05) serum T-SOD and Cu-Zn SOD activities than that in the ZnSO₄ group. This study indicated that supplementation of Zn in basal diet improved productive and reproductive performance, Zn concentration and antioxidant status in broiler breeders, and the 80 mg Zn/kg from Zn-Gly was the optimum choice for broiler breeders compared with other levels of Zn from Zn-Gly and 80 mg/kg Zn from ZnSO₄.     

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

INTRODUCTIONZinc is essential for normal brain development,evidenced by the fact that zinc deficiency in lactating mothers is characterized by a high incidence ofneuroanatomical maiformatinns and functional abnormalities in suckling offspring[1-3]. By colltrast,relatively little is known about the relationship be{tween maternal zinc nutrition and fetal brain development[2, 4, 5]. Dvergsten et al[6-81 investigated theeffects of maternal zinc deficiency on postnatal development of the rat ce…     

Calibrated Forceps Model of Spinal Cord Compression Injury

Compression injuries of the murine spinal cord are valuable animal models for the study of spinal cord injury (SCI) and spinal regenerative therapy. The calibrated forceps model of compression injury is a convenient, low cost, and very reproducible animal model for SCI. We used a pair of modified forceps in accordance with the method published by Plemel et al. (2008) to laterally compress the spinal cord to a distance of 0.35 mm. In this video, we will demonstrate a dorsal laminectomy to expose the spinal cord, followed by compression of the spinal cord with the modified forceps. In the video, we will also address issues related to the care of paraplegic laboratory animals. This injury model produces mice that exhibit impairment in sensation, as well as impaired hindlimb locomotor function. Furthermore, this method of injury produces consistent aberrations in the pathology of the SCI, as determined by immunohistochemical methods. After watching this video, viewers should be able to determine the necessary supplies and methods for producing SCI of various severities in the mouse for studies on SCI and/or treatments designed to mitigate impairment after injury.     

不同频率电针刺激对神经痛模型大鼠脊髓背角P物质的影响

目的:观察P物质(Substance P,SP)在慢性坐骨神经压迫损伤(chronic constriction injury,CCI)模型脊髓中表达的变化,探讨电针镇痛的机制是否与脊髓背角中SP表达的变化有关。方法:选择32只雄性、体重180-200 g的SD大鼠,并将其随机均分为4组(n=8)。空白组(Con组)为正常痛阈值大鼠;假电针组(CCI+A组)在损伤的坐骨神经旁置入电针,但无电流刺激;2 Hz组和100Hz组分别给予相应频率电流刺激30 min。在实验开始前和术后1、4、7、14、20、22天记录大鼠的热缩足反射潜伏期(Paw Withdrawal Latency,PWL)和机械刺激缩足反射阈值(Paw Withdrawal Threshold,PWT)。免疫组化方法检测脊髓背角SP的表达。结果:术后20天,电针治疗后,100 Hz组和2 Hz组PWT分别为(7.33±1.42)g和(7.80±1.42)g,均显著高于假电针组(2.60±1.46)g,差异有统计学意义(P0.05)。100 Hz组在术后20天后和2 Hz组在术后14天后PWL值均显著高于假电针组,差异有统计学意义(P0.05)。免疫组化显示:2 Hz组和100 Hz组大鼠脊髓背角中P物质阳性细胞显著低于假电针组(P0.05)。结论:坐骨神经旁电针刺激能够显著减轻CCI模型大鼠热痛觉及机械痛觉过敏,其机制可能与抑制脊髓背角SP的表达有关。     

Combination of Dexamethasone and Aminoguanidine Reduces Secondary Damage in Compression Spinal Cord Injury

The study was performed to investigate the effect of combination therapy with aminoguanidine (AG) and dexamethasone (DEX) on the compression spinal cord injury (SCI) in rat. Compared to the control group, the combination therapy group with AG (75 mg/kg) and DEX (0.025 mg/kg) significantly reduced the degree of (1) spinal cord edema, (2) the permeability of blood spinal cord barrier (measured by ^99mTc-Albumin), (3) infiltration of neutrophils (MPO evaluation), (4) cytokines expression (tumor necrosis factor-α and interleukin-1β), and (5) apoptosis (measured by Bax and Bcl-2 expression). In addition, we have also clearly demonstrated that the combination therapy significantly ameliorated the recovery of limb function (evaluated by motor recovery score). Taken together, our results clearly indicated for the first time that strategies targeting multiple proinflammatory pathways may be more effective than a single effector molecule for the treatment of SCI.     

Monoaminergic Modulation of Spinal Viscero-Sympathetic Function in the Neonatal Mouse Thoracic Spinal Cord

Descending serotonergic, noradrenergic, and dopaminergic systems project diffusely to sensory, motor and autonomic spinal cord regions. Using neonatal mice, this study examined monoaminergic modulation of visceral sensory input and sympathetic preganglionic output. Whole-cell recordings from sympathetic preganglionic neurons (SPNs) in spinal cord slice demonstrated that serotonin, noradrenaline, and dopamine modulated SPN excitability. Serotonin depolarized all, while noradrenaline and dopamine depolarized most SPNs. Serotonin and noradrenaline also increased SPN current-evoked firing frequency, while both increases and decreases were seen with dopamine. In an in vitro thoracolumbar spinal cord/sympathetic chain preparation, stimulation of splanchnic nerve visceral afferents evoked reflexes and subthreshold population synaptic potentials in thoracic ventral roots that were dose-dependently depressed by the monoamines. Visceral afferent stimulation also evoked bicuculline-sensitive dorsal root potentials thought to reflect presynaptic inhibition via primary afferent depolarization. These dorsal root potentials were likewise dose-dependently depressed by the monoamines. Concomitant monoaminergic depression of population afferent synaptic transmission recorded as dorsal horn field potentials was also seen. Collectively, serotonin, norepinephrine and dopamine were shown to exert broad and comparable modulatory regulation of viscero-sympathetic function. The general facilitation of SPN efferent excitability with simultaneous depression of visceral afferent-evoked motor output suggests that descending monoaminergic systems reconfigure spinal cord autonomic function away from visceral sensory influence. Coincident monoaminergic reductions in dorsal horn responses support a multifaceted modulatory shift in the encoding of spinal visceral afferent activity. Similar monoamine-induced changes have been observed for somatic sensorimotor function, suggesting an integrative modulatory response on spinal autonomic and somatic function.     

Depletion of vesicular zinc in dorsal horn of spinal cord causes increased neuropathic pain in mice

Zinc enriched (ZEN) neurons and terminals are abundant in the rodent spinal cord. Zinc ions have been suggested to modulate the excitability of primary afferent fibers believed to be important in nociceptive transmission. To test the hypothesis that vesicular zinc concentration is related to neuropathic pain we applied Chung’s rodent pain model on BALB/c mice, and traced zinc transporter 3 (ZnT3) proteins and zinc ions with immunohistochemistry and autometallography (AMG), respectively. Under anesthesia the left fifth lumbar spinal nerve was ligated in male mice in order to produced neuropathic pain. The animals were then sacrificed 5 days later. The ZnT3 immunoreactivity was found to have decreased significantly in dorsal horn of fourth, fifth, and sixth lumbar segments. In parallel with the depressed ZnT3 immunoreactivity the amount of vesicular zinc decreased perceptibly in superficial gray matters of especially layer I-IV of the same segments. The transection-induced reduction of vesicular zinc in ZEN terminals of the dorsal horn was synchronic to reduced pain threshold, as measured by von Frey method. In a separate study, we observed intensive zinc selenite precipitation in somata of the smaller spinal ganglion cell, but 5 days after spinal nerve transection zinc precipitation was also found in the lager ganglion cells. The present results indicate that zinc may be involved in pain mechanism in the spinal ganglion level. These results support the hypothesis that vesicular zinc might have a modulatory role for neuropathic pain. Thus, increased pain sensitivity might be related to reduce vesicular zinc level in the dorsal spinal gray matter.     

The Correlation Among the Dynamic Change of Zn<Superscript>2+</Superscript>, ZnT-1, and Brain-Derived Neurotrophic Factor After Acute Spinal Cord Injury in Rats

Zinc plays an important role in regulating the expression of brain-derived neurotrophic factor (BDNF) and its receptor in nervous system, but the correlation among Zn²⁺, zinc transporter, and BDNF in spinal cord injuries (SCI) is not fully understood. The purpose of this study was to investigate the expression of Zn²⁺, zinc transporter 1 (ZnT-1), and BDNF, as well as their correlation in spinal cord-injured rats. One hundred Wistar male rats were divided into two groups: sham-operated group (as control group) and model group. Spinal cord injury was induced in model groups by hemisection of T9 on the left side. Compared with the control group, the serum zinc levels in SCI model group were significantly decreased after surgery, but zinc concentrations in spinal cord were increased gradually. The mRNA levels of ZnT-1 and BDNF were significantly increased in SCI model group, and there is a positive correlation between them (Spearman rho = 0.381, P = 0.0204). The correlation found between BDNF and ZnT-1 allows us to speculate that these two factors may be physiologically co-regulated, which may provide an idea for the treatment of SCI.     

Effect of Zinc Source on Performance, Zinc Status, Immune Response, and Rumen Fermentation of Lactating Cows

Two experiments were conducted to examine the effect of zinc (Zn) source on the performance, Zn status, immune response, and rumen fermentation of lactating cows to find the most available Zn source for dairy production. In Experiment 1, a total of 30 multiparous Holstein cows were randomly allocated by body weight and milk yield to one of five treatments in a completely randomized design. Cows were fed a total mixed ration (TMR) with no Zn addition (containing 37.60 mg?Zn/kg TMR by analysis), and the basal TMR supplemented with 40 mg?Zn/kg TMR from either Zn sulfate or one of three organic Zn chelates with weak (Zn-AA W), moderate (Zn-Pro M), or strong (Zn-Pro S) chelation strengths, respectively for 55 days. In Experiment 2, the in vitro rumen fermentation method was used in a completely randomized design involving a 4?×?3 factorial arrangement of treatments. The four Zn sources were the same as those used in Experiment 1, and the three supplemental Zn levels in the rumen fluid were 0, 10, and 20 μg/mL, respectively. The feed intake, milk composition, and somatic cell count (SCC) were unaffected (P?>?0.05) by treatments. However, the milk yield was increased (P?<?0.05) by addition of Zn from both the Zn-AA W and Zn-Pro S. Plasma Zn level at the end of the experiment was increased (P?<?0.05) by addition of Zn from all three organic sources. Serum antibody titers on day 21 after vaccination with foot and mouth disease (FMD) vaccine were increased (P?<?0.05) by both supplemental Zn-AA W and Zn-Pro S. The organic Zn sources with different chelation strengths supplemented at the added Zn level of 10 μg/mL were more effective (P?<?0.05) in improving the rumen fermentation than Zn sulfate, with the most effective being Zn-AA W. In conclusion, Zn source had no influence on the feed intake, milk composition, and SCC; however, both the Zn-AA W and Zn-Pro S were more effective than Zn-Pro M and Zn sulfate in enhancing the rumen fermentation, Zn status, and humoral immune response as well as improving milk yield of lactating cows. The improved milk production might be attributed to the improved rumen fermentation, Zn status, and immune function.     

Neuroprotective Effects of Ebselen on Experimental Spinal Cord Injury in Rats

Spinal cord injury (SCI) results in rapid and significant oxidative stress. This study was aimed to investigate the possible beneficial effects of Ebselen in comparison with Methylprednisolone in experimental SCI. Thirty six Wistar albino rats (200–250 g) were divided in to six groups; A (control), B (only laminectomy), C (Trauma; laminectomy + spinal trauma), D (Placebo group; laminectomy + spinal trauma + serum physiologic), E (Methylprednisolone group; laminectomy + spinal trauma + Methylprednisolone treated), F (Ebselen group; laminectomy + spinal trauma + Ebselen treated), containing 6 rats each. Spinal cord injury (SCI) was performed by placement of an aneurysm clip, extradurally at the level of T11–12. After this application, group A, B and C were not treated with any drug. Group D received 1 ml serum physiologic. Group E received 30 mg/kg Methylprednisolone and, Group F received 10 mg/kg Ebselen intraperitoneally (i.p.). Rats were neurologically examined 24 h after trauma and spinal cord tissue samples had been harvested for both biochemical and histopathological evaluation. All rats were paraplegic after SCI except the ones in group A and B. Neurological scores were not different in traumatized rats than that of non-traumatized ones. SCI significantly increased spinal cord tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities compared to control. Methylprednisolone and Ebselen treatment decreased tissue MDA and PC levels and prevented inhibition of the enzymes SOD, GSH-Px and CAT in the tissues. However, the best results were obtained with Ebselen. In groups C and D, the neurons of the spinal cord tissue became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in groups E and F were very well protected, but not as good as the control group. The number of neurons in the spinal cord tissues of the groups C and D were significantly less than the groups A, B, E and F. We concluded that the use of Ebselen treatment might have potential benefits in spinal cord tissue damage on clinical grounds.     

Association Between Zinc, Copper, and Iron Concentrations in Breast Milk and Growth of Healthy Infants in Tabriz, Iran

The aims of this study were to determine the effect of breast milk zinc, copper, and iron concentrations on infants’ growth and their possible correlations with maternal dietary intake. Milk samples and information on food intake were collected from 182 lactating women. Concentrations of zinc, copper, and iron in milk were analyzed using atomic absorption spectrophotometry. The infant’s weight for age Z-score (WAZ) and height for age Z-score (HAZ) were calculated. The mean milk zinc, copper, and iron concentrations were 1.85?±?0.5, 0.53?±?0.3, and 0.85?±?0.2 mg/l, respectively. Only zinc mean level was lower than the recommended range. Association between zinc, copper, and iron concentrations of milk and WAZ or HAZ of infants were not significant. However, the WAZ of infants whose mothers' milk zinc was more than 2 mg/l was significantly (P?<?0.039) higher than for others. The mean dietary zinc (5.31?±?2.3 mg/day) and copper (1.16?±?0.7 mg/day) intake of mothers was significantly less than the required daily intake (RDA) recommendations (P?<?0.05). The mean dietary iron intake (11.8?±?8.2 mg/day) was significantly higher than RDA recommendation (P?<?0.001). No significant association was found between maternal mean dietary zinc, copper, and iron intakes with their concentrations in milk. Dietary consultation or/and zinc supplementation is suggested for lactating women and infants.     

Differential Roles of Phosphorylated AMPA Receptor GluR1 Subunits at Serine-831 and Serine-845 Sites in Spinal Cord Dorsal Horn in a Rat Model of Post-Operative Pain

Previous studies have demonstrated that the enhanced levels of phosphorylated α-amino-3-hydroxy-5-methy-4-isoxazole propionate (AMPA) receptor GluR1 subunits at Serine-831 (pGluR1-Ser-831) and Serine-845 (pGluR1-Ser-845) in the spinal cord dorsal horn are involved in central sensitization of inflammatory pain. However, whether the phosphorylatory regulation of AMPA receptor GluR1 subunits is implicated in the development and maintenance of post-operative pain remains unclear. The current study aims to examine the functional regulation of AMPA receptor GluR1 subunit through its phosphorylation mechanism during the period of post-operative painful events in rats. Our data indicated that the expression of pGluR1-Ser-831 in ipsilateral spinal cord dorsal horn increased significantly at 3 h after incision, then decreased gradually, and returned to the normal level 3 day post-incision. Meanwhile, the expression of pGluR1-Ser-845 and GluR1 in ipsilateral spinal cord dorsal horn remained unchanged. The cumulative pain scores increased at 3 h after incision, gradually decreased afterwards and returned to the baseline values at 4 day after incision and the trend was almost parallel to the expression changes of pGluR1-Ser-831 in spinal dorsal horn. Intrathecal injection of a calcium-dependent protein kinase (PKC) inhibitor, Gö6983 (10 μM), significantly reversed the incision-mediated over-expression of pGluR1-Ser-831 in spinal dorsal horn at 3 h after incision and decreased the cumulative pain scores as well. These results indicate that the phosphorylation of GluR1 subunits at Serine-831 and Serine-845 sites might be differentially regulated following surgical procedures and support a neurobiological mechanism of post-operative pain involved in phosphorylation of AMPA subunits GluR1-Ser-831, but not pGluR1-Ser-845. Our study suggests that the therapeutic targeting the phosphorylation regulation of AMPA receptor GluR1 subunit at Serine-831 site would be potentially significant for treating postoperative pain.