Protective Effect Of Zinc Research Articles

Protective effect of zinc against A2E-induced toxicity in ARPE-19 cells: Possible involvement of lysosomal acidification

A key pathogenic mechanism of dry age-related macular degeneration (AMD) is lysosomal dysfunction in retinal pigment epithelium (RPE) cells, which results in the accumulation of lipofuscins such as A2E (N-retinylidene-N-retinylethanolamine) that further compromises lysosomal function. This vicious cycle leads to cell death and poor visual acuity. Here, we established an in vitro model of AMD by treating a human RPE cell line (ARPE-19) with A2E and examined whether raising zinc levels confers protective effects against lysosomal dysfunction and cytotoxicity. MTT assay showed that A2E induced apoptosis in ARPE-19 cells. pHrodo™ Red fluorescence staining showed that lysosomal pH increased in A2E-treated ARPE-19 cells. Treatment with a zinc ionophore (clioquinol) reduced A2E accumulation, restored lysosomal pH to the acidic range, and reduced A2E-induced cell death, all of which were reversed by the addition of a zinc chelator (TPEN). Consistent with the in vitro results, subretinal injections of A2E in mouse eyes resulted in the death of RPE cells as well as lysosomal dysfunction, all of which were reversed by co-treatment with clioquinol. Our results suggest that restoring the levels of intracellular zinc, especially in lysosomes, would be helpful in mitigating A2E-induced cytotoxic changes including lysosomal dysfunction in RPE cells in the pathogenesis of AMD.

Zinc deficiency increases lung inflammation and fibrosis in obese mice by promoting oxidative stress

BackgroundZinc deficiency can lead to multiple organ damage. In this study, we investigated the effects of zinc deficiency on obesity-related lung damage. MethodsC57BL/6 J mice were fed a diet with differing amounts of zinc and fat over a 6-month period. Palmitic acid was used to stimulate A549 cells to construct a high-fat alveolar epithelial cell model. Western blotting and histopathological staining were performed on animal tissues. Nuclear expression of nuclear factor erythroid 2-related factor 2 (Nrf2) was detected in cultured cells. A reactive oxygen species (ROS) assay kit was used to detect intracellular ROS. Furthermore, Nrf2 siRNA was used to examine zinc deficiency effects on A549 cells. ResultsPathological results showed significant damage to the lung structure of mice in the high-fat and low-zinc diet group, with a significant increase in the expression of inflammatory (IL-6, TNF-α) and fibrosis (TGFβ1, PAI-1) factors, combined with a decrease in the expression of Nrf2, HO-1 and NQO1 in the antioxidant pathway. In A549 cells, high fat and low zinc levels aggravated ROS production. Western blot and immunofluorescence results showed that high fat and zinc deficiency inhibited Nrf2 expression. After Nrf2-specific knockout in A549 cells, the protective effect of zinc on oxidant conditions induced by high fat was reduced. Phosphorylated Akt and PI3K levels were downregulated on the high-fat and low-zinc group compared with the high-fat group. ConclusionsZinc attenuated lung oxidative damage in obesity-related lung injury and Nrf2 activation is one of the important mechanisms of this effect. General significanceRegulating zinc homeostasis through dietary modifications or supplemental nutritional therapy can contribute to the prevention and treatment of obesity-related lung injury.

Does the Protective Effect of Zinc on Telomere Length Depend on the Presence of Hypertension or Type 2 Diabetes? Results from the Iwaki Health Promotion Project, Japan.

Telomeres, repeated TTAGGG sequences at chromosomal ends, shorten with age and indicate cellular lifespan. Zinc can protect against telomere damage through its anti-oxidative effect. Meanwhile, telomere shortening was correlated with metabolic diseases of hypertension and type 2 diabetes. The objective of this study was to investigate whether the association between zinc and telomere length differs by the presence or absence of hypertension/type 2 diabetes. This is a cross-sectional study with 1064 participants of the Iwaki area, Japan. Multiple linear regression models were performed to test the hypothesis. A higher serum zinc concentration was significantly associated with a longer G-tail length (β = 48.11, 95% confidence intervals [CI]: 25.69, 70.54, p < 0.001). By multivariate linear regression analysis, there was a significant positive association between zinc and G-tail length in both hypertensive (β = 46.84, 95%CI: 9.69, 84.0, p = 0.014) and non-hypertensive groups (β = 49.47, 95%CI: 20.75, 78.18, p = 0.001), while the association was significant only in the non-diabetes group (β = 50.82, 95%CI: 27.54, 74.11, p < 0.001). In conclusion, higher zinc concentration was significantly associated with longer G-tail length. The protective effect of zinc on G-tail did not differ by hypertension status; however, it disappeared in individuals with type 2 diabetes.

Determination of Corrosion Rate in Galvanized Pipes in Centralized Hot Water Supply Systems

To counteract possible corrosion, steel pipes are coated with a protective layer of zinc with a thickness of 20 to 85 microns, depending on the requirements of regulatory documentation. It is proven that hot-deposited zinc can effectively protect steel surfaces for 20 to 120 years. However, in centralized hot water supply (CHWS) systems, the period of protective action can decrease to two to three years, with further damage to the zinc layer and the appearance of fistulas. In order to counteract adverse factors, it is necessary to take into account the operating mode and design features of the system, the properties of the coating, and the environment in which the pipes operate. In this article, the main attention is paid to the study of the behavior of zinc coating. The protective properties and corrosion rate of zinc coating in tap water were evaluated. It was established that the protective effect of zinc is effectively manifested in the ratio of the protected area to the unprotected, as SZn/SFe ≥ 9:1. The influence of iron-containing sediment, when it accumulates in the pipes of a CHWS system, on the corrosion rate of the zinc coating was studied. It was also noted that the corrosion rates of the new zinc coating and uncoated steel pipe measured in short-term tests differed slightly.

The protective effect of zinc, selenium, and chromium on myocardial fibrosis in the offspring of rats with gestational diabetes mellitus.

The offspring of gestational diabetes mellitus (GDM) mothers are considered to be at the risk of cardiovascular diseases due to intrauterine hyperglycemia exposure. Our previous study showed that zinc, selenium, and chromium dramatically alleviated glucose intolerance in GDM rats and their offspring (P < 0.05). However, the effects of these elements on the damage of the cardiac myocytes of GDM offspring and the underlying mechanisms have not been demonstrated. Here, we investigated the beneficial effects of zinc (10 mg per kg bw), selenium (20 μg per kg bw), and chromium (20 μg per kg bw) supplementation on myocardial fibrosis in the offspring of GDM rats induced by a high-fat and sucrose (HFS) diet. The results showed that maternal GDM induced glucose intolerance, oxidative stress, cardiac inflammation and myocardial fibrosis in offspring rats during different ages (3 days, 3 weeks, and adulthood), which were ameliorated by zinc, selenium and chromium supplementation (P < 0.05). The activity of cardiac damage markers such as creatine kinase-myocardial band isoenzyme (CK-MB), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) decreased by 40-60% in element-supplemented offspring compared to that in non-supplemented offspring of GDM dams (P < 0.05). Moreover, maternal GDM-induced expression of fibrosis-related proteins and the transforming growth factor-beta 1 (TGF-β1)/small mothers against decapentaplegic homolog 3 (Smad3) signaling pathway in the heart tissue of offspring was down-regulated by zinc, selenium, and chromium supplementation (P < 0.05). In conclusion, zinc, selenium, and chromium may play a protective role in maternal GDM-induced myocardial fibrosis in offspring from birth to adulthood by inactivating the TGF-β1/Smad3 pathway.

Zinc normalizes hepatic lipid handling via modulation of ADA/XO/UA pathway and caspase 3 signaling in highly active antiretroviral therapy-treated Wistar rats

BackgroundAlthough highly active antiretroviral therapy (HAART) is effective in the management of HIV, it has been reported to induce hepatic injury and non-alcoholic fatty liver (NAFLD). However, there is a lack of data on the roles of the adenosine deaminase (ADA)/xanthine oxidase (XO)/uric acid (UA) pathway and caspase 3 signaling in HAART-induced NAFLD. Also, whether or not zinc confers protection against HAART-induced NAFLD is not known. AimThis study evaluated the involvement of the ADA/XO/UA pathway and caspase 3 signaling in HAART-induced hepatic lipid accumulation. It also evaluated the possible protective effect of zinc in HAART-induced hepatic lipid accumulation and injury. MethodsThirty two male Wistar rats (n = 8/group) were assigned into four groups namely; vehicle-treated (p.o), zinc-treated (3 mg/kg/day of elemental zinc; p.o), HAART-treated (a cocktail of 52.9 mg/kg of Efavirenz, 26.48 mg/kg of Lamivudine, and 26.48 mg/kg of Tenofovir; p.o), and HAART + zinc-treated groups. The treatment lasted for 8 weeks. ResultsHAART administration led to increased body weight and hepatic weight, but unaltered hepatic organo-somatic index. HAART exposure also resulted in impaired glucose homeostasis, evidenced by increased fasting blood glucose, hyperinsulinemia, and insulin resistance (IR), increased plasma and hepatic cholesterol and triglycerides, and impaired hepatic function as depicted by elevated hepatic injury markers and reduced glycogen synthase activity and glycogen content. These findings were accompanied by increased plasma and hepatic ADA and XO activities, UA and malondialdehyde levels, inflammatory markers, and caspase 3 activities. However, HAART suppressed plasma and hepatic antioxidant defenses. Furthermore, HAART distorted hepatic histoarchitecture and reduced hepatic sinusoidal diameter. Co-administration of zinc with HAART normalized HAART-induced alterations. ConclusionsThese findings showed that downregulation of the ADA/XO/UA pathway and caspase 3 signalings may rescue the liver from HAART-induced lipid accumulation and injury.

The protective effect of zinc and its relationship with some hematological, biochemical, and histological parameters in adult male rats

The protective effect of zinc and its relationship with some hematological, biochemical, and histological parameters in adult male rats

Extracellular Oxidative Stress Markers in COVID-19 Patients with Diabetes as Co-Morbidity.

COVID-19 patients have a higher risk of developing inflammatory responses associated with serious and even fatal respiratory diseases. The role of oxidative stress in exacerbating manifestations in COVID-19 pathogenesis is under-reported.This study aimed touseserum levels of superoxide dismutase (SOD3) and glutathione-S-transferase (GSTp1) by ELISA, zinc (ErbaChem5), ferritin and free iron (VitrosChemistry, Ortho Clinical Diagnosis, Raritan, NJ, USA) at the first encounter of randomly selected RT-PCR-positive COVID-19 patients, for assessing disease severity. The parameters which helped in identifying the severity, leading to poor prognosis, were neutrophil:lymphocyte higher than 4, high CRP, low SOD3 values and high GSTp1 values, and diabetes mellitus as a co-morbidity. Higher zinc levels correlated with high GSTp1 and low SOD3, indicating the protective effect of zinc on ROS. The increased high GSTp1 shows an anticipated protective biochemical response, to mitigate the low SOD3 values due to ROS consumption. Decreased SOD3 levels indicate a state of high oxidative stress at cellular levels, and an anticipated increase in GSTp1 levels points to the pathophysiological bases of increasing severity with age, sex, and co-morbidities, such asdiabetes. High levels of initial GSTp1 and zinc levels possibly offer protection to redox reactions at the cellular level in severe COVID-19 infection, preventing deterioration.

Protective Effects of Zinc on Salmonella Invasion, Intestinal Morphology and Immune Response of Young Pigeons Infected with Salmonella enterica Serovar Typhimurium.

The study aimed to determine the effects of orally supplemental zinc on body weight, Salmonella invasion, serum IgA, intestinal histomorphology, and immune response of Salmonella enterica serovar Typhimurium (S. typhimurium)-challenged young pigeons. A total of 72 healthy White King pigeons (25days old) with similar weight were randomly assigned to 3 treatments with six replicate cages. The 3 treatments were unchallenged, S. typhimurium-challenged, and S. typhimurium-challenged orally supplemented with 1mg zinc per bird. Salmonella infection decreased (P < 0.05) the body weight, the bursa index, the serum IgA content, and the villus height/crypt depth ratio in the ileum, but increased the neutrophil proportion (P < 0.001) and the mRNA expressions of IL-1β and IL-8 in the jejunum (P < 0.05). Orally supplemental zinc reduced (P = 0.007) the bacterial load in the liver and improved (P < 0.05) the body weight, the bursa index, the serum IgA content, the villus height/crypt depth ratio, and the NOD-like receptor family pyrin domain containing 3 (NLRP3) protein expression, as well as tended to increase (P = 0.064) the protein abundance of caspase-1 of the jejunum, but did not alleviate the high level of neutrophil proportion and IL-1β mRNA expression of the jejunum (P > 0.05). The results indicated that oral zinc supplementation improved the intestinal mucosal morphology and enhanced the immune response, as well as activated caspase-1-dependent cell pyroptosis pathways in the jejunal epithelium, thereby restricting Salmonella invasion of the challenged young pigeons.

Retraction Note to: Deoxynivalenol-induced alterations in the redox status of HepG2 cells: identification of lipid hydroperoxides, the role of Nrf2-Keap1 signaling, and protective effects of zinc.

Retraction Note to: Deoxynivalenol-induced alterations in the redox status of HepG2 cells: identification of lipid hydroperoxides, the role of Nrf2-Keap1 signaling, and protective effects of zinc.

Protective Effects of Zinc on Spinal Cord Injury.

Spinal cord injury is a serious disease of the central nervous system, but there is no effective treatment. And zinc is an essential nutrient for human body and participates in many physiological processes, such as immune response, homeostasis, oxidative stress, cell cycle progression, DNA replication, DNA damage repair, apoptosis, and aging. This article mainly summarizes that zinc could predict the prognosis and treat the spinal cord injury. Especially, zinc could help to inhibit inflammation, regulate autophagy, and reduce oxidative stress. However, excessive zinc will damage neurons.

Evaluation of Body Weight, Serum Lipid Profile, Glucose Homeostasis, Oxidative Stress and Hepatic Function in Healthy Mice Fed With Zinc Sulphate Supplementation

The present research study was designed to evaluate the effect of zinc supplementation on body weight, serum triglyceride, cholesterol, glucose homeostasis, oxidative stress, and hepatic function in mice. Mice were treated with zinc sulphate at an equivalent weight of 6.5 mg/kg-body weight elemental zinc for four weeks. Bodyweight, serum glucose, triglyceride, cholesterol, serum MDA, nitric oxide, vitamin C, and hepatic enzymes level were determined at the end of the study period. Data from this study showed that supplementation with zinc in mice maintained a balanced blood glucose homeostasis throughout the experimental period. Moreover, treatment with zinc showed a significant (p &lt;0.05) decrease in serum triglyceride and cholesterol level along with a decrease in the body weight compared to control. Treatment with zinc significantly attenuated the rate of lipid peroxidation whereas increased the level of vitamin C and NO level. The protective effect of zinc on liver activity was observed. Treatment with zinc showed a strong negative association with serum total cholesterol (r= -0.934, p = 0.02), triglycerides level (r= -0.709, p = 0.05), and body weight (r= -0.899, p = 0.01). The present findings demonstrate that zinc supplementation can be helpful to maintain a glucose homeostasis, ameliorate hyperlipidemia, oxidative stress, and liver dysfunction. Therefore, zinc supplementation can be suggested to alleviate diseases associated with metabolic syndrome and oxidative stress.&#x0D; Dhaka Univ. J. Pharm. Sci. 20(1): 59-66, 2021 (June)

The protective effect of zinc on morphine-induced testicular toxicity via p53 and Akt pathways: An in vitro and in vivo approach

BackgroundChronic use of morphine is associated with reproductive complications, such as hypogonadism and infertility. While the side effects of morphine have been extensively studied in the testis, much less is known regarding the effects of morphine on Sertoli cells and the effects of zinc on morphine-induced testicular injury as well as their underlying mechanisms. Therefore, the purpose of this study was to investigate the effect of morphine (alone and co-administered with zinc) on cell viability and apoptosis of the testicular (Sertoli) cells as well as the tumor suppressor p53 and phosphorylated-protein kinase B (p-Akt) protein levels in both in vitro and in vivo models. MethodsCultured Sertoli cells were exposed to morphine (23 μM), zinc (8 μM), and zinc prior to morphine and their effects on Sertoli cell viability and apoptosis were investigated. Morphine (3 mg/kg) and zinc (5 mg/kg, 1 h before morphine) were also injected intraperitoneally to rats and then the apoptotic changes in the testis were evaluated. ResultsCell viability and p-Akt protein levels decreased in morphine-treated cells, while apoptosis and p53 protein expression increased in these cells. Pretreatment with zinc recovered morphine-induced apoptotic effects, as well as over-expression of p53 and down-regulation of p-Akt. These findings were supported by a subsequent animal study. ConclusionThe present data indicated the protective effect of zinc against morphine-induced testicular (Sertoli) cell toxicity via p53/Akt pathways in both in vivo and in vitro models and suggested the clinical importance of zinc on infertility among chronic opioid users and addicted men.

Protective effect of zinc and Pine barks extract supplement against Indometacin-induced gastric ulcer in rats

Abstract This investigation was aimed to study the effect of Pinus halepensis aqueous bark extract and zinc to prevent indomethacin induced gastric ulcer in rats. Thirty female albino Wistar rats were divided into 6 groups of 5 animals each (n=5); Group 1: normal control, Group 2: ulcer rats received normal saline, Group 3: ulcer rats treated with P. halepensis, Group 4: ulcer rats were treated with zinc, Group 5: ulcer rats were treated with P. halepensis + zinc and Group 6 ulcer rats were treated with Ranitidine for 15 days. Stomach ulcer was induced by a single oral administration of indomethacin (30 mg/kg). Various biochimical, physiologic and histologic parameters were estimated. Obtained results show that the ulcer index, pH and total acidity level were significantly reduced (p&lt;0.05) and Pepsin activity was significantly increased (p&lt; 0.05) in ulcer induced rats pre-treated with extract of P. halepensis, zinc and ranitidine when compared with indomethacin treated rats. The MDA level was significantly decreased and GSH level was increased (p&lt; 0.05) in rats treated with plant extract and zinc. Histopathology of gastric mucosa confirmed the gastro-protection by plant and zinc treatment. The study reveals anti-ulcer and antioxidant properties were observed in bark aqueous extract of P. halepensis groups with a benefic effect of zinc to reduce oxidative stress and gastric ulcer induced in the rat.

Zinc offers splenic protection through suppressing PERK/IRE1-driven apoptosis pathway in common carp (Cyprinus carpio) under arsenic stress

Arsenic (As) occurs naturally and concentrations in water bodies can reach high levels, leading to accumulation in vital organs like the spleen. Being an important organ in immune response and blood development processes, toxic effects of As on the spleen could compromise immunity and cause associated disorders in affected individuals. Splenic detoxification is key to improving the chances of survival but relatively little is known about the mechanisms involved. Essential trace elements like zinc have shown immune-modulatory effects humans and livestock. This study aimed to investigate the mechanisms involved in As-induced splenic toxicity in the common carp (Cyprinus carpio), and the protective effects of zinc (Zn). Our findings suggest that environmental exposure to As caused severe histological injuries and Ca2+ accumulation in the spleen of common carp. Additionally, transcriptional and translational profiles of endoplasmic reticulum stress, apoptosis and autophagy-related genes of the spleen showed upward trends under As toxicity. Treatment with Zn appears to offer protection against As-induced splenic injury in common carp and the pathologic changes above were alleviated. Our results provide additional insight into the mechanism of As toxicity in common carp while elucidating the role of Zn, a natural immune-modulator, as a potential antidote against As poisoning.

Deoxynivalenol-induced alterations in the redox status of HepG2 cells: identification of lipid hydroperoxides, the role of Nrf2-Keap1 signaling, and protective effects of zinc.

Deoxynivalenol (DON) is a type B trichothecenes that is widely contaminating human and animal foods, leading to several toxicological implications if ingested. Induction of oxidative stress and production of lipid peroxides were suggested to be the reasons for DON-induced cytotoxicity. However, detailed and comprehensive profiling of DON-related lipid hydroperoxides was not identified. Furthermore, the mechanisms behind DON-induced cytotoxicity and oxidative stress have received less attention. Zinc (Zn) is an essential element that has antioxidant activities; however, the protective effects of Zn against DON-induced adverse effects were not examined. Therefore, this study was undertaken to investigate DON-induced cytotoxicity and oxidative damage to human HepG2 cell lines. Furthermore, a quantitative estimation for the formed lipid hydroperoxides was conducted using LC-MS/MS. In addition, DON-induced transcriptomic changes on the inflammatory markers and antioxidant enzymes were quantitatively examined using qPCR. The protective effects of Zn against DON-induced cytotoxicity and oxidative stress, the formation of lipid hydroperoxides (LPOOH), and antioxidant status in HepG2 cells were investigated. Finally, the effects of DON and Zn on the Nrf2-Keap1 pathway were further explored. The achieved results indicated that DON caused significant cytotoxicity in HepG2 cells accompanied by significant oxidative damage and induction of the inflammatory markers. Identification of DON-related LPOOH revealed the formation of 22 LPOOH species including 14 phosphatidylcholine hydroperoxides, 5 triacylglycerol hydroperoxides, and 3 cholesteryl ester hydroperoxides. DON caused significant downregulation of Nrf2-regulated antioxidant enzymes. Zn administration led to significant protection of HepG2 cells against DON-induced adverse effects, probably via activation of the Nrf2-Keap1 pathway.

Mercury toxicity in pregnant and lactating rats: zinc and N-acetylcysteine as alternative of prevention.

This study evaluated the toxic effects of inorganic mercury (Hg) in pregnant and lactating rats, as well as the possible protective effect of zinc (Zn) and N-acetylcysteine (NAC). Pregnant and lactating rats were pre-treated with ZnCl2 (27mg/kg) and/or NAC (5mg/kg) and after 24h, they were exposed to HgCl2 (10mg/kg). Animals were sacrificed 24h after Hg exposure, and biochemical tests and metal determination were performed. Regarding pregnant rats, Hg exposure caused kidney, blood, and placenta δ-aminolevulinic acid dehydratase (δ-ALA-D) activity inhibition, and the pre-treatments showed a tendency of protection. Moreover, all the animals exposed to Hg presented high Hg levels in the kidney, liver, and placenta when compared with control group. Pregnant rats pre-exposed to Zn (Zn-Hg and Zn/NAC-Hg groups) presented an increase in hepatic metallothionein levels. Therefore, lactating rats exposed to Hg presented renal and blood δ-ALA-D inhibition; the pre-treatments showed a tendency to prevent the renal δ-ALA-D inhibition and prevented the blood δ-ALA-D inhibition caused by Hg. Lactating rats exposed to Hg presented high Hg levels in the kidney and liver. These results showed that 10mg/kg of HgCl2 causes biochemistry alterations in pregnant and lactating rats, and Zn and NAC present promising results against these damages.

Low-dose heavy metal mixture (lead, cadmium and mercury)-induced testicular injury and protective effect of zinc and Costus afer in wistar albino rats.

The study evaluated the protective effect of Costus afer on low-dose heavy metal mixture (LDHMM)-mediated effects in the testis of albino rats. The weight-matched animals were divided into six groups: normal control, metal mixture of (PbCl2 +CdCl2 + HgCl2 ), combination of metal mixture+Costus afer at 750mg/kg, combination of metal mixture+Costus afer at 1,500mg/kg, combination of metal mixture+Costus afer at 2,250mg/kg and combination of metal mixture + (ZnCl2 ). LDHMM reduced (p<.05) the antioxidant biomarkers (superoxide dismutase, SOD; catalase, CAT; and glutathione, GSH) and increased (p<.05) the lipid peroxidation marker (malondialdehyde, MDA) and lead, cadmium and mercury concentrations in the testis. Treatment with LDHMM increased (p<.05) abnormal sperm morphology and plasma prolactin (PRL) level and decreased epididymal sperm count, viability, follicle-stimulating hormone (FSH), luteinising hormone (LH) and testosterone. LDHMM exposure caused deleterious changes in the testis. Treatment of rats with Costus afer (750, 1,500 and 2,250mg/kg) dose-dependently reduced (p<.05) the LDHMM-mediated toxicity. Treatment with Costus afer also reversed the testicular weight and LDHMM decrease in antioxidant biomarkers. Costus afer may be a defensive modulator of LDHMM-mediated testicular lesions.

Protective effects of zinc on rat sperm chromatin integrity involvement: DNA methylation, DNA fragmentation, ubiquitination and protamination after bleomycin etoposide and cis-platin treatment

Testicular cancer is one of the most common malignancy in young men, chemotherapy induced damage in cancerous cells as well as healthy tissue, and we decided to investigate recovery effect of zinc (Zn) on chemotherapy-induced complications in rat chromatin integrity and testicular histomorphometry. The male rats (n = 40) were treated with BEP at appropriate dose levels of BEP (0.75, 7.5, and 1.5 mg/kg) for 9 weeks, with or without Zn; testicular histology, sperm DNA methylation, ubiquitination, DNA fragmentation and protamination were further assessed through immunofluorescence. BEP treatment significantly increased ubiquitination, and DNA fragmentation, considerably reducing global DNA methylation and protamination (P < 0.001), resulting in degenerative changes in testicular structure. Zn restored normal DNA methylation, protamination and structure of male gonads, maintained spermatogonial stem cells, and significantly reduced the mean percentage of ubiquitination and sperm DNA fragmentation as compared with BEP group (P < 0.001). We found that supplementation of Zn following chemotherapy can improve chromatin integrity, testicular organization and spermatogenesis.

Zinc treatment modulates hematological and morphological changes in rat erythrocytes following arsenic exposure.

The aim of this study was to understand the effects of zinc supplementation on antioxidant defense systems, hematological indices, and erythrocyte morphology in conditions of chronic arsenic toxicity. Male Wistar rats were segregated into four groups: control, arsenic treated, zinc supplemented, and arsenic + zinc treated. The animals in the arsenic-treated group were given arsenic orally in drinking water in the form of sodium arsenite at a dose level of 100 mg L-1, and zinc was administered to zinc-treated animals in the form of zinc sulfate orally in drinking water at a dose level of 227 mg L-1. The animals were subjected to different treatments for a period of 12 weeks, and various investigations were undertaken that included serum zinc content, activity of antioxidant enzymes, and hematological indices. Further, scanning electron microscopic (SEM) studies were performed to assess morphological changes in erythrocytes. Arsenic treatment significantly reduced serum zinc concentrations, which, however, were restored to near-normal levels upon zinc supplementation. The activities of enzymes involved in antioxidant defense systems were altered in the erythrocyte lysates of arsenic-treated rats, which interestingly revealed a significant improvement upon simultaneous zinc supplementation. A significant reduction in the counts of total leukocytes, neutrophils, and lymphocytes was observed following arsenic intoxication, which came back to near control levels following zinc supplementation. Also, protective effects of zinc were evident from SEM that revealed maintenance of topographical appearances of erythrocytes in conditions of arsenic toxicity. Thus, this study clearly shows the protection afforded by zinc on erythrocytes during arsenic-induced toxicity.