The Effect of Chronic Swimming Exercise and Vitamin E Supplementation on Bone Element Metabolism in Epileptic Rats.

Introduction: This study aimed to investigate the effects of chronic swimming exercise and vitamin E administration on elemental levels in the bone tissue of epileptic rats. Methods: Forty-eight rats were divided into six groups: Control, Swimming, Swimming + vitamin E, Swimming + Epilepsy, Swimming + Epilepsy + vitamin E, and Epilepsy. Vitamin E was administered to the animals chronically by gavage at a dose of 500 mg/kg every other day for 3 months. Epileptiform activity was induced with penicillin in animals 24 hours after the last vitamin E intake. The exercise program consisted of daily 30-minute swimming sessions. At the end of the treatment period, the levels of calcium, chromium, copper, iron, magnesium, manganese, lead, and zinc (µg/gram tissue) in bone tissue samples were measured using an atomic emission device. Results: The results showed that all epileptic groups had significantly lower bone chromium levels compared to the control groups (p<0.05). The epileptic, and epileptic swimming groups had the lowest levels of bone calcium, magnesium, and zinc (p<0.05). Vitamin E administration resulted in a significant increase in bone calcium, magnesium, and zinc levels in the epileptic swimming group with vitamin E compared to the epileptic and epileptic swimming groups. (p<0.05). Conclusion: The findings of the study show that the administration of vitamin E improves calcium, magnesium, and zinc metabolism in the deteriorated bone tissue of the epileptic rat model.

Zinc Supplementation Improves ZIP14 (SLC39A14) Levels in Cerebral Cortex Suppressed by icv-STZ Injection.

Introduction: Metabolic dysfunctions are critical in the pathology of Alzheimer's disease. Impaired zinc homeostasis, in particular, is a significant issue in this disease that has yet to be explained. Gene expression of ZIP14 in brain tissue has been previously reported. But to date, only one study has reported reduced ZIP14 levels in aged brain tissue. We investigated how dietary zinc deprivation and supplementation impact ZIP14 levels in the cerebral cortex in rats with sporadic Alzheimer's disease (sAH) produced by intracerebroventricular streptozotocin (icv-STZ). Impaired zinc homeostasis, in particular, is a significant issue with this condition that has yet to be elucidated. Methods: Animals were divided into 5 groups in equal numbers (n=8): Sham 1 group: icv received artificial cerebrospinal fluid (aCSF); Sham 2 group: retrieved icv aCSF and intraperitoneal (ip) saline, STZ group: received 3 mg/kg icv-STZ; STZ-Zn-Deficient group: received 3 mg/kg icv-STZ and fed a zinc-deprived diet; STZ-Zn-Supplemented: It received 3 mg/kg icv-STZ and ip zinc sulfate (5 mg/kg/day ZIP 14 levels (ng/L) in cortex tissue samples taken from animals sacrificed under general anesthesia were determined by ELISA at the final stage of the experimental applications. Results: Decreased ZIP14 levels in the sporadic Alzheimer's group were severely by zinc deficiency. Zinc supplementation treated the reduction in ZIP14 levels. Conclusion: The results of the current study show that ZIP14 levels in cerebral cortex tissue, which are suppressed in the experimental rat Alzheimer model and are even more critically reduced in zinc deficiency, can be restored by zinc supplementation.

Marginal Maternal Zinc Deficiency Produces Liver Damage and Altered Zinc Transporter Expression in Offspring Male Rats.

The aim of this study was to investigate how zinc deficiency and supplementation affect liver markers including autotaxin, kallistatin, endocan, and zinc carrier proteins ZIP14 and ZnT9 in rats exposed to maternal zinc deficiency. Additionally, the study aimed to assess liver tissue damage through histological examination. A total of forty male pups were included in the research, with thirty originating from mothers who were given a zinc-deficient diet (Groups 1, 2, and 3), and the remaining ten born to mothers fed a standard diet (Group 4). Subsequently, Group 1 was subjected to a zinc-deficient diet, Group 2 received a standard diet, Group 3 received zinc supplementation, and Group 4 served as the control group without any supplementation. Upon completion of the experimental phases of the study, all animals were sacrificed under general anesthesia, and samples of liver tissue were obtained. The levels of autotaxin, kallistatin, endocan, ZIP 14, and ZnT9 in these liver tissue samples were determined using the ELISA technique. In addition, histological examination was performed to evaluate tissue damage in the liver samples. In the group experiencing zinc deficiency, both endocan and autotaxin levels increased compared to the control group. With zinc supplementation, the levels of endocan and autotaxin returned to the values observed in the control group. Similarly, the suppressed levels of kallistatin, ZIP14, and ZnT9 observed in the zinc deficiency group were reversed with zinc supplementation. Likewise, the reduced levels of kallistatin, ZIP14, and ZnT9 seen in the zinc deficiency group were rectified with zinc supplementation. Moreover, the application of zinc partially ameliorated the heightened liver tissue damage triggered by zinc deficiency. This study is the pioneering one to demonstrate that liver tissue dysfunction induced by a marginal zinc-deficient diet in rats with marginal maternal zinc deficiency can be alleviated through zinc supplementation.

The impact of flavonoids and BDNF on neurogenic process in various physiological/pathological conditions including ischemic insults: a narrative review.

OBJECTIVE: Ischemic stroke is the leading cause of mortality and disability worldwide with more than half of survivors living with serious neurological sequelae thus, it has recently attracted considerable attention in the field of medical research. Neurogenesis is the process of formation of new neurons in the brain, including the human brain, from neural stem/progenitor cells [NS/PCs] which reside in neurogenic niches that contain the necessary substances for NS/PC proliferation, differentiation, migration, and maturation into functioning neurons which can integrate into a pre-existing neural network.Neurogenesis can be modulated by many exogenous and endogenous factors, pathological conditions. Both brain-derived neurotrophic factor, and flavonoids can modulate the neurogenic process in physiological conditions and after various pathological conditions including ischemic insults. AIMS: This review aims to discuss neurogenesis after ischemic insults and to determine the role of flavonoids and BDNF on neurogenesis under physiological and pathological conditions with a concentration on ischemic insults to the brain in particular. METHOD: Relevant articles assessing the impact of flavonoids and BDNF on neurogenic processes in various physiological/pathological conditions including ischemic insults within the timeline of 1965 until 2023 were searched using the PubMed database. CONCLUSIONS: The selected studies have shown that ischemic insults to the brain induce NS/PC proliferation, differentiation, migration, and maturation into functioning neurons integrating into a pre-existing neural network. Flavonoids and BDNF can modulate neurogenesis in the brain in various physiological/pathological conditions including ischemic insults. In conclusion, flavonoids and BDNF may be involved in post-ischemic brain repair processes through enhancing endogenous neurogenesis.

The relationship between beta cell activation and SLC30A8/ZnT8 levels of the endocrine pancreas and maternal zinc deficiency in rats.

OBJECTIVES: Zinc, which is found in high concentrations in the ß-cells of the pancreas, is also a critical component for the endocrine functions of the pancreas. SLC30A8/ZnT8 is the carrier protein responsible for the transport of zinc from the cytoplasm to the insulin granules. The aim of this study was to investigate how dietary zinc status affects pancreatic beta cell activation and ZnT8 levels in infant male rats born to zinc-deficient mothers. METHODS: The study was performed on male pups born to mothers fed a zinc-deficient diet. A total of 40 male rats were divided into 4 equal groups. Group 1: In addition to maternal zinc deficiency, this group was fed a zinc-deficient diet. Group 2: In addition to maternal zinc deficiency, this group was fed a standard diet. Group 3: In addition to maternal zinc deficiency, this group was fed a standard diet and received additional zinc supplementation. Group 4: Control group. Pancreas ZnT8 levels were determined by ELISA method and insulin-positive cell ratios in ß-cells by immunohistochemistry. RESULTS: The highest pancreatic ZnT8 levels and anti-insulin positive cell ratios in the current study were obtained in Group 3 and Group 4. In our study, the lowest pancreatic ZnT8 levels were obtained in Group 1 and Group 2, and the lowest pancreatic anti-insulin positive cell ratios were obtained in Group 1. CONCLUSION: The results of the present study; in rats fed a zinc-deficient diet after maternal zinc deficiency has been established shows that ZnT8 levels and anti-insulin positive cell ratios in pancreatic tissue, which is significantly suppressed, reach control values with intraperitoneal zinc supplementation.

Melatonin protects retinal tissue damage in streptozotocin-induced aged rats.

OBJECTIVES: The aim of this study was to investigate how melatonin administration affects retinal oxidative damage and retinal SIRT1 gene activation in diabetic elderly female rat model. METHODS: 16-months-old female rats were used in the study. A total of 24 rats were divided into 4 groups in equal numbers: Group 1. Control, Group 2. Control + Melatonin, Group 3. Diabetes, Group 4. Diabetes + Melatonin. In group 3 and 4 rats, diabetes was induced by intraperitoneal (IP) injection of streptozotocin. Groups 2 and 4 were given ip melatonin for 4 weeks. SIRT-1 gene expression was determined by PCR method and GSH and MDA levels by ELISA in retinal tissue samples taken from animals sacrificed under general anesthesia. RESULTS: In our study, the highest retinal SIRT1 expression values were obtained in the diabetes + melatonin (G4) group. The retinal SIRT1 expression values of the diabetes group (G3) were lower than group 4 and higher than the general control (G1) and control + melatonin (G2) groups. Again in our study, the highest retinal MDA values were obtained in the diabetes group (G3). The highest retinal GSH values were obtained in the Diabetes + melatonin group (G4). CONCLUSION: The results of our study showed that melatonin supplementation has a protective effect on retinal tissue in a diabetic elderly female rat model. This protective effect of melatonin supplementation occurs by increasing both retinal antioxidant activity and retinal SIRT1 gene expression.

Cardiovascular Diseases and Zinc.

Zinc is structurally and functionally essential for more than 300 enzymes and 2000 transcription factors in human body. Intracellular labile zinc is the metabolically effective zinc and tiny changes in its concentrations significantly affect the intracellular signaling and enzymatic responses. Zinc is crucial for the embrionic and fetal development of heart. Therefore, it is shown to be related with a variety of congenital heart defects. It is involved in epithelial-to-mesenchymal transformation including endocardial cushion development, which is necessary for atrioventricular septation as well as the morphogenesis of heart valves. In atherosclerosis, monocyte endothelial adhesion, and diapedesis, activation and transformation into macrophages and forming foam cells by the ingestion of oxidized LDL are monocyte related steps which need zinc. Intracellular zinc increases intracellular calcium through a variety of pathways and furthermore, zinc itself can work as a second messenger as calcium. These demonstrate the significance of intracellular zinc in heart failure and arterial hypertension. However, extracellular zinc has an opposite effect by blocking calcium channels, explaining decreased serum zinc levels, contrary to the increased cardiomyocyte and erythrocyte zinc levels in hypertensive subjects. These and other data in the literature demonstrate that zinc has important roles in healthy and diseased cardiovascular system but zinc-cardiovascular system relationship is so complex that, it has not been explained in all means. In this article, we try to review some of the available knowledge about this complex relationship.

Zinc Ameliorates Nogo-A Receptor and Osteocalcin Gene Expression in Memory-Sensitive Rat Hippocampus Impaired by Intracerebroventricular Injection of Streptozotocin.

Metabolic dysfunction is a critical step in the etiopathogenesis of Alzheimer's disease. In this progressive neurological disorder, impaired zinc homeostasis has a key role that needs to be clarified. The aim of this study was to investigate the effect of zinc deficiency and administration on hippocampal Nogo-A receptor and osteocalcin gene expression in rats injected with intracerebroventricular streptozotocin (icv-STZ). Forty male Wistar rats were divided into 5 groups in equal numbers: Sham 1 group received icv artificial cerebrospinal fluid (aCSF); Sham 2 group received icv a CSF and i.p. saline; STZ group received 3 mg/kg icv STZ; STZ-Zn-deficient group received 3 mg/kg icv STZ and fed a zinc-deprived diet; STZ-Zn-supplemented group received 3 mg/kg icv STZ and i.p. zinc sulfate (5 mg/kg/day). Hippocampus tissue samples were taken following the cervical dislocation of the animals under general anesthesia. Nogo-A receptor and osteocalcin gene expression levels were determined by real-time-PCR method. Zinc supplementation attenuated the increase in hippocampal Nogo-A receptor gene expression, which was significantly increased in zinc deficiency. Again, zinc supplementation upregulated the intrinsic protective mechanisms of the brain by activating osteocalcin-expressing cells in the brain. The results of the study show that zinc has critical effects on Nogo-A receptor gene expression and hippocampal osteocalcin gene expression levels in the memory-sensitive rat hippocampus that is impaired by icv-STZ injection. These results are the first to examine the effect of zinc deficiency and supplementation on hippocampal Nogo-A receptor and osteocalcin gene expression in icv-STZ injection in rats.

Lithium promotes long-term neurological recovery after spinal cord injury in mice by enhancing neuronal survival, gray and white matter remodeling, and long-distance axonal regeneration.

Spinal cord injury (SCI) induces neurological deficits associated with long-term functional impairments. Since the current treatments remain ineffective, novel therapeutic options are needed. Besides its effect on bipolar mood disorder, lithium was reported to have neuroprotective activity in different neurodegenerative conditions, including SCI. In SCI, the effects of lithium on long-term neurological recovery and neuroplasticity have not been assessed. We herein investigated the effects of intraperitoneally administered lithium chloride (LiCl) on motor coordination recovery, electromyography (EMG) responses, histopathological injury and remodeling, and axonal plasticity in mice exposed to spinal cord transection. At a dose of 0.2, but not 2.0 mmol/kg, LiCl enhanced motor coordination and locomotor activity starting at 28 days post-injury (dpi), as assessed by a set of behavioral tests. Following electrical stimulation proximal to the hemitransection, LiCl at 0.2 mmol/kg decreased the latency and increased the amplitude of EMG responses in the denervated hindlimb at 56 dpi. Functional recovery was associated with reduced gray and white matter atrophy rostral and caudal to the hemitransection, increased neuronal survival and reduced astrogliosis in the dorsal and ventral horns caudal to the hemitransection, and increased regeneration of long-distance axons proximal and distal to the lesion site in mice receiving 0.2 mmol/kg, but not 2 mmol/kg LiCl, as assessed by histochemical and immunohistochemical studies combined with anterograde tract tracing. Our results indicate that LiCl induces long-term neurological recovery and neuroplasticity following SCI.

Chronic Running Exercise Regulates Cytotoxic Cell Functions and Zinc Transporter SLC39A10/ZIP10 Levels in Diabetic Rats.

The aim of this study is to investigate how chronic running exercise affects ZIP10 levels in thymus and spleen tissue as well as immune parameters in diabetic rats. A total of 40 adult male Wistar rats were divided into 4 equal groups: group 1, control; group 2, exercise control; group 3, diabetes; group 4, diabetes + exercise. Diabetes was induced by injecting intraperitoneal streptozotocin (STZ) at a dose of 40 mg/kg twice with 24-h intervals to the animals in groups 3 and 4. The animals in group 2 and group 4 underwent exercise for 45 min on the rat treadmill for 4 weeks at 20 m/min. Twenty-four hours after the last running exercise, the animals were sacrificed under general anesthesia. Immunological parameters were determined by flow cytometric method; tissue ZIP 10 levels were determined by ELISA method. The diabetic group had the lowest natural killer (NK) and natural killer T (NKT) cells percentages. Chronic exercise partially improved NK and NKT cell percentages in diabetic rats. The diabetic group had the lowest ZIP10 levels in spleen and thymus tissue. ZIP10 values in spleen and thymus tissue of diabetes exercise group were significantly higher than diabetes group. The results of our study show that the impaired cytotoxic cell functions in diabetes are partially corrected with 4 weeks of chronic exercise, and that the suppressed ZIP 10 levels in diabetic rats are reversed by 4 weeks of chronic exercise.

The Role of Zinc Status on Spatial Memory, Hippocampal Synaptic Plasticity, and Insulin Signaling in icv-STZ-Induced Sporadic Alzheimer's-Like Disease in Rats.

Alzheimer's disease (AD), especially its sporadic form (sAD), is of multifactorial nature. Brain insulin resistance and disrupted zinc homeostasis are two key aspects of AD that remain to be elucidated. Here, we investigated the effects of dietary zinc deficiency and supplementation on memory, hippocampal synaptic plasticity, and insulin signaling in intracerebroventricular streptozotocin (icv-STZ)-induced sAD in rats. The memory performance was evaluated by Morris water maze. The expression of hippocampal protein and mRNA levels of targets related to synaptic plasticity and insulin pathway was assessed by Western blot and real-time quantitative PCR. We found memory deficits in icv-STZ rats, which were fully recovered by zinc supplementation. Western blot analysis revealed that icv-STZ treatment significantly reduced hippocampal PSD95 and p-GSK3ß, and zinc supplementation restored the normal protein levels. mRNA levels of BDNF, PSD95, SIRT1, GLUT4, insulin receptor, and ZnT3 were found to be reduced by icv-STZ and reestablished by zinc supplementation. Our data suggest that zinc supplementation improves cognitive deficits and rescues the decline in key molecular targets of synaptic plasticity and insulin signaling in hippocampus caused by icv-STZ induced sAD in rats.

The effects of thyroid dysfunction on DNA damage and apoptosis in liver and heart tissues of rats.

OBJECTIVES: Thyroid hormones affect many enzymes, organs, and systems. They also play a role in complex biological events including development and growth. The main objective of this study was to analyze the effects of thyroid dysfunction on DNA damage and apoptosis in liver and heart tissues as well as the treatment of these disorders. METHODS: Thirty-eight Wistar-albino male rats were randomly divided into five groups: 1. Control group (n=6): The rats were sacrificed without any application and liver and heart samples were collected. 2. Hypothyroidism group (n=8): Prophyltiouracil (PTU)-10 mg/kg/day was applied to induce hypothyroidism by intraperitoneal route for two weeks. 3. Hypothyroidism + Thyroxine group (n=8): After one week of PTU application (10 mg/kg/day), a high dose of l-thyroxine (1.5 mg/kg/day) was applied by intraperitoneal route for one week. 4. Hyperthyroidism group (n=8): l-thyroxine (0.3 mg/kg/day) was applied intraperitoneally to induce hyperthyroidism for two weeks. 5. Hyperthyroidism + PTU group (n=8): After one week of high dose l-thyroxine application, PTU (10 mg/kg/day) was applied for one week. RESULTS: Liver and heart tissues were collected to evaluate 8-hydroxy-2 deoxyguanosine (8-OHdG), caspase-8 and caspase-9 levels. Hypothyroidism caused DNA damage in the liver, while hyperthyroidism caused DNA damage in the heart tissue. Hyperthyroidism also led to a significant increase in levels of caspase-8 and caspase-9 in liver tissue. CONCLUSIONS: The results of the study show that DNA damage and caspase levels in the heart and liver are affected differently in experimental hypothyroidism and hyperthyroidism.

The Effect of Zinc and Melatonin Administration on Lipid Peroxidation, IL-6 Levels, and Element Metabolism in DMBA-Induced Breast Cancer in Rats.

The purpose of this study was to investigate the effects of zinc and melatonin administration on interleukin-6, lipid peroxidation parameters, and element metabolism in DMBA-induced breast cancer in female rats. A total of 42 recently weaned Wistar rats were divided into 5 groups as follows: control (group 1), DMBA control (group 2), DMBA + zinc (group 3), DMBA + melatonin (group 4), and DMBA + melatonin and zinc (group 5). Malondialdehyde (MDA) and glutathione (GSH) levels in breast tissue and blood samples were determined via spectrophotometric methods. In addition, iron, magnesium, zinc, and copper levels in serum samples were determined by atomic emission, and plasma interleukin-6 levels were determined by ELISA method. The highest tissue and plasma MDA and the lowest tissue and erythrocyte GSH levels found in the study were in group 2; the highest tissue and erythrocyte GSH levels and the lowest tissue and plasma MDA levels are in group 5 (P < 0.05). Iron, magnesium, and zinc levels of groups 3, 4, and 5 were higher than the DMBA group without administration (group 2), but the copper values were significantly lower (P < 0.05). The highest IL-6 levels were determined in group 2 while IL-6 levels in the DMBA group (G5) treated with combined melatonin and zinc were lower than all other breast cancer groups (P < 0.05). According to the findings obtained in this presented study, combined zinc and melatonin therapy can contribute to the prevention of tumor growth by improving the disruption in element metabolism and suppressing IL-6 levels and reducing tissue damage that causes the cancer.

The effect of thyroid dysfunction and treatment on adropin, asprosin and preptin levels in rats.

OBJECTIVES: Thyroid hormones have important roles in normal development and energy regulating mechanisms as well as signaling mechanisms that affect energy consumption through central and peripheral pathways. The aim of this study was to determine the effects of thyroid dysfunction on adropin, asprosin and preptin levels in rat. METHODS: The study was performed on the 38 male Wistar-albino rats. Experiment groups were designed as follows. 1-Control, 2-Hypothyroidism; To induce hypothyroidism PTU was applied by intraperitoneal as 10 mg/kg/day for 2 weeks. 3-Hypothyroidism + Thyroxine; Previously animals were made with hypothyroidism by 1 week PTU application and then 1 week l-thyroxine was given by intraperitoneal as 1.5 mg/kg/day. 4-Hyperthyroidism; Rats were made with hyperthyroidism by 3 weeks l-thyroxine (0.3 mg/kg/day). 5-Hyperthyroidism + PTU; Animals were made hyperthyroisim by l-thyroxine as groups 4, then 1 week PTU was applied to treatment of hiperthyrodism. At the end of supplementation animals were sacrificed and blood samples were collected for FT3, FT4, adropin, asprosin, preptin analysis. RESULTS: FT3 ve FT4 levels were reduced significantly in hypothyroidism while increased in hyperthyroidism (p<0.001). Hipothyrodism led to reduces adropin, asprosin and preptin levels. And also hyperthyroidism reduced adropin and preptin levels (p<0.001). CONCLUSIONS: The results of study show that experimental hypothyroidism and hyperthyroidism lead to significantly change to adropin, asprosin and preptin levels. However, correction of thyroid function caused to normals levels in asprosin and preptin.

Effect of resveratrol administration on muscle glycogen levels in rats subjected to acute swimming exercise.

The present study aims to examine how resveratrol administration affects muscle glycogen levels in rats subjected to an acute swimming exercise bout. The study was conducted on adult male rats of Wistar-Albino. The 28 rats used in the study were equally divided among four groups: Group 1, Control Group: The group fed on a standard diet and not subjected to any procedure. Group 2, Control Swimming Group: The group fed on a standard diet and subjected to an acute swimming exercise bout for 30 minutes at the end of the study. Group 3, Resveratrol Group: The group fed on a standard diet and given (10 mg/kg) resveratrol in drinking water for four weeks. Group 4, Resveratrol + Swimming Group: The group fed on a standard diet, given (10 mg/kg) resveratrol in drinking water for four weeks and subjected to a 30-minute acute swimming exercise at the end of the study. At the end of the four weeks, the animals were decapitated, muscle glycogen levels using immunohistochemical method. The highest muscle glycogen levels were obtained in the resveratrol-administered Group 3 and the lowest levels in group 2 (swimming group) (p<0.05). The results of the study demonstrate that resveratrol support had a protective and/or regulatory effect on mucle glycogen in both exercised and not-exercised rats.

Effects of morning and nocturnal soccer matches on levels of some trace elements in young trained males.

The aim of this study was to comparatively evaluate effect of morning and nocturnal soccer matches induced metabolic stress on plasma levels of iron (Fe), copper (Cu) and zinc (Zn). Twenty male footballers performed two soccer matches in morning and at night on different days. Blood samples were taken before and after match. The levels of Fe, Zn and Cu were measured through an atomic absorption spectrophotometry. Metabolic stress was evaluated by altered malondialdehyde (MDA) levels that measured using High Performance Liquid Chromatography. In morning and at nocturnal soccer matches, levels of MDA (36% and 27%), Fe (37.4% and 38.9%) and Cu (34.8% and 26.8%) were all increased in all subjects, respectively. However, Zn level decreased -4.5 % in morning (n=10 subjects) and -9.4% at nocturnal (n=12 subjects) soccer matches. In addition, Cu/Zn ratio increased significantly 46.6% in morning and 36.6% at nocturnal soccer matches. Soccer match has significant effects on levels of MDA, Fe and Cu but not Zn levels. The results of this study showed that morning soccer match significantly alters levels of MDA and Cu and Cu/Zn ratio compared to nocturnal soccer match.

Review: The role of zinc in the endocrine system.

Zinc is essential in the regulation of a variety of physiological and biochemical events in the organism. It plays a critical role in maintaining the cell membrane integrity, protein-carbohydrate-lipid metabolism, immune system, wound injury and in the regulation of a number of other biological processes associated with normal growth and development. Physiological and biochemical levels of many hormones are affected by zinc metabolism. Therefore, growth impairment, hypogonadism, and some endocrine diseases are associated with the deficiency of zinc. These effects of zinc are considered versatile. Zinc increases the synthesis of the growth hormone and its number of receptors; thus, it is an important mediator in the binding of this hormone to its receptor. Found in a large quantity in the pancreas tissue, zinc has a part in the regulation of the effect of insulin. Zinc is involved to much more thyroid hormone metabolism such as hormone synthesis, receptor activity, conversion of T4 to T3, and production of carrier proteins. The low levels of zinc and high levels of leptin in obese individuals point to a critical relationship between zinc and leptin. Zinc is related to enzyme activity to melatonin synthesis. Melatonin has regulatory activity for zinc absorption from gastrointestinal system. Zinc particularly affects the conversion of testosterone to dihydrotestosterone, as 5α-reductase that is involved in this conversion is a zinc-dependent enzyme. In consideration of these relations, zinc is accepted to play critical roles in the endocrine system. The aim of the current review is to draw attention to the effects of zinc on the endocrine system.

Molecular Mechanisms of Early and Late LTP.

LTP is the most intensively studied cellular model of the memory and generally divided at least two distinct phases as early and late. E-LTP requires activation of CaMKII that initiates biochemical events and trafficking of proteins, which eventually potentiate synaptic transmission, and is independent of de novo protein synthesis. In contrast, L-LTP requires gene expression and local protein synthesis regulated via TrkB receptor- and functional prions CPEB2-3-mediated translation. Maintenance of LTP for longer periods depends on constitutively active PKMζ. Throughout this review, current knowledge about early and late phases of LTP will be reviewed.

Melatonin has a protective effect against lipid peroxidation in the bone tissue of diabetic rats subjected to acute swimming exercise.

Aim The present study aimed to examine the effects of melatonin supplementation on lipid peroxidation in the bone tissue of diabetic rats subjected to acute swimming exercise. Methods The study was conducted on 80 Sprague-Dawley type adult male rats which were equally allocated to eight groups: group 1, general control; group 2, melatonin-supplemented control; group 3, melatonin-supplemented diabetic control; group 4, swimming control; group 5, melatonin-supplemented swimming; group 6, melatonin-supplemented diabetic swimming; group 7, diabetic swimming; group 8, diabetic control. In order to induce diabetes, the animals were subcutaneously injected with 40 mg/kg streptozotocin (STZ). The animals were supplemented with 3 mg/kg/day melatonin intraperitoneally (IP) for 4 weeks. At the end of the study, the animals were decapitated to collect bone tissue samples which were examined to find out the malondialdehyde (MDA) (nmol/g/protein) and glutathione (GSH) (mg/dL/g protein) levels. Results The highest MDA values in the bone tissue were found in groups 7 and 8. MDA levels in the bone tissue in groups 3 and 6 were lower than the levels in groups 7 and 8, but higher than those in all other groups. Groups 3, 5 and 6 had the highest bone tissue GSH values. On the other hand, the lowest GSH level was established in groups 7 and 8. Conclusion The results of the present study indicated that the cell damage caused by acute swimming exercise and diabetes in the bone tissue could be prevented by melatonin supplementation.

The effect of zinc and melatonin supplementation on immunity parameters in breast cancer induced by DMBA in rats.

OBJECTIVE: The aim of the study was to determine the effects of zinc and melatonin supplements on the immunity parameters of female rats with breast cancer induced by DMBA. METHODS: Group 1; Control, Group 2; 7,12-dimethylbenz[a]anthracene (DMBA), Group 3; DMBA + zinc, Group 4; DMBA + melatonin, Group 5; DMBA + zinc + melatonin. The rats' breast cancer was induced by DMBA 80 mg/kg. Groups 3-5 received daily 5 mg/kg doses of zinc, melatonin, and zinc + melatonin, respectively. Lymphocyte rates, T-lymphocyte subgroups, B-lymphocyte and natural killer cells (NK), and natural killer T (NKT) were evaluated. RESULTS: The most significant increase in lymphocyte, T-lymphocyte, and CD4 lymphocyte rates was found in Group 5. The highest NKT cell rates were found in Group 3. CONCLUSIONS: Findings show that zinc and melatonin supplements have led to an increase in the immunity parameters of rats with breast cancer.