Form Of Zinc Sulphate Research Articles

Morphological, biochemical and molecular characterization of twelve nitrogen-fixing bacteria and their response to various zinc concentration.

Background:Zinc is an essential micronutrient used in the form of zinc sulfate in fertilizers in the agriculture production system. Nitrogen-fixing microorganisms are also of considerable value in promoting soil fertility.Objectives:This study aimed to investigate the degree of sensitivity to varying concentrations of zinc, in the form of ZnSO4, in different strains of Azotobacter chroococcum in a laboratory environment.Materials and Methods:To isolate A. chroococcum strains, soil samples were collected from wheat, corn and asparagus rhizospheres and cultured in media lacking nitrogen at 30˚C for 48 hours. Strains were identified based on morphological and biochemical characteristics. The presence of the nitrogenase enzyme system was confirmed by testing for the presence of the nifH gene using PCR analysis. The minimum inhibitory concentration (MIC) and optimal zinc concentration for the growth of each strain was determined.Results:A total of 12 bacterial strains were isolated from six different soil samples. A. chroococcum strains were morphologically and biochemically characterized. The presence of the nifH gene was confirmed in all the strains. MIC and the optimal zinc concentration for bacterial growth were 50 ppm and 20 ppm, respectively.Conclusions:It was concluded that increasing the concentration of zinc in the agricultural soil is harmful to beneficial microorganisms and reduces the soil fertility. A 20-ppm zinc concentration in soil is suggested to be optimal.

Identification of ten N2-fixing bacteria using 16S rRNA and their response to various zinc concentrations

Zinc is presently being used as a micronutrient essential for plant growth in agriculture in the form of zinc sulphate in fertilizers. Considering the importance of nitrogen-fixing microorganisms in soil fertility and plant growth, and the toxic effects of zinc, this study aimed at isolating nitrogen-fixing microorganisms from the asparagus rhizosphere arable soil and examining the sensitivity of the isolated strains to different zinc concentrations. The asparagus rhizosphere soil was cultivated in a nitrogen-free environment at 30 °C for 48 hours. Strains were identified by both biochemical and molecular methods. The presence of the nitrogenase enzyme system was confirmed by testing for the presence of the nifH gene through PCR analysis. The minimum inhibitory concentration (MIC) and optimal zinc concentration for the growth of each strain were also determined. A total of 10 different bacterial species were identified in three different soil samples. The presence of the nifH gene was confirmed in seven different strains. MIC and the average optimal zinc concentration for bacterial growth were 130.7 ppm and 13 ppm, respectively. The asparagus rhizosphere soil contains different species of nitrogen stabilizing microorganisms. An optimal zinc concentration in soil of 20 ppm is suggested.

Effect of boron and zinc fertilization on white oats grown in soil with average content of these nutrients

The objective of this study was to evaluate the effect of fertilization with zinc or boron on the growth and dry matter production, nutritional value and accumulation of nutrients in white oats. The study comprised two experiments conducted in glasshouses, the first consisting of the application of four doses of zinc (0, 0.2, 0.4 and 0.6 mg/dm3) in the form of zinc sulphate (20% Zn), and the second consisting of the application of four doses of boron (0, 0.2, 0.4 and 0.6 mg/dm3) in the form of Borax (11% B). The experimental design in each case was a randomized block design, with five replicates. Fertilization with zinc and boron increased the growth of white oats, but had no significant effect on the nutritional value of the forage. Higher levels of absorption and accumulation of nutrients in plant tissues were observed following the application of boron and zinc at rates of up to 0.60 mg/dm3 of soil.

Influence of long-term crop management practices on grain yield and incidence of brown planthopper in rice

A correct ratio between organic and inorganic sources of nutrients is essential to ensure optimum yield in any crop, including rice. A long-term experiment to study the influence of organic and inorganic nutrient sources on rice yield started in the 1991 kharif season at ARS, Siruguppa, in the Tungabhadra project area of Karnataka, India. The experiment was laid out in a randomized block design with four replications at a fixed site. Different levels of inorganic fertilizers (NPK), organic sources (farmyard manure, Gliricidia, Sesbania), and plant population were included as treatments (see table). A common dose of zinc (at 20 kg ha -1 ) in the form of zinc sulfate was applied to all treatments. Rice variety BPT-5204 was planted every kharif season at 20 × 10-cm spacing, except in treatments where 25% more seedlings were transplanted, which used a spacing of 15 × 10 cm. Brown planthopper (BPH) was recorded in the 1999 kharif season 90 d after transplanting (DAT) on 10 hills in each treatment and computed per hill. Both grain yield and BPH population data were subjected to statistical analysis.

Regulatory Role of Zinc on the Biokinetics and Biodistribution of 65Zn During the Initiation of Experimentally Induced Colon Cancer

The present study was conducted to evaluate the kinetics of zinc utilization during the formation of colon carcinoma in an animal model of colon carcinogenesis. The rats were segregated into 4 groups: untreated control, 1,2 dimethylhydrazine (DMH) treated, zinc treated, and DMH+zinc treated. Colon carcinogenesis was initiated through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 8 wk. Zinc (in the form of zinc sulphate) was supplemented at a dose level of 227mg/L in drinking water, ad libitum for the entire duration of study. Whole body 65Zn kinetics followed two-compartment kinetics, with Tb1 representing the initial fast component of the biological half-life and Tb2, the slower component. The Tb1 component showed a significant elevation while the Tb2 component was significantly diminished in DMH-treated rats, which, however, got normalized following zinc supplementation. The biodistribution and subcellular distribution of 65Zn was significantly affected in DMH-treated rats when compared to normal control rats. However, zinc significantly reversed the altered 65Zn uptake in different organs and various fractions of colon. The present study for the first time demonstrated a faster mobilization of zinc during initiation of experimentally induced colon carcinoma and provides a physiological basis for the role of zinc in colon tumorigenesis.

In Vitro 14C-Labeled Amino Acid Uptake Changes and Surface Abnormalities in the Colon after 1,2-Dimethylhydrazine—Induced Experimental Carcinogenesis: Protection by Zinc

The present study explored the regulatory role of zinc on the in vitro uptake of ¹⁴C-glucose and ¹⁴C-labeled amino acids and on colonic surface abnormalities after 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis. Rats were segregated into four groups: control, DMH-treated, zinc-treated, and DMH + zinc-treated. Colon carcinogenesis was induced through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 16 weeks. Zinc (in the form of zinc sulfate) was given to rats at a dose level of 227 mg/L in their drinking water. DMH treatment caused a significant decrease in the activities of disaccharidases (sucrase, lactase, and maltase), but a significant increase in the activity of alkaline phosphatase. In vitro uptake of ¹⁴C-D-glucose and the amino acids ¹⁴C-glycine, ¹⁴C-alanine, ¹⁴C-lysine, and ¹⁴C-leucine were significantly higher in the colons of DMH-treated rats. Zinc supplementation of DMH-treated rats resulted in regulating the altered intestinal enzyme activities and in vitro uptake of ¹⁴C-amino acids and ¹⁴C-glucose. Scanning electron microscopy revealed drastic alterations in the colon surface morphology after DMH treatment, which were restored after zinc supplementation. Our results confirm a beneficial effect of zinc against DMH-induced alterations in the colons of rats.

Toxicidade do zinco em milheto cultivado em Latossolo Vermelho Distrófico

Zinc toxicity causes nutritional disorders specific for millet plants, damaging dry matter production. The objective of this experiment was to evaluate the effects of zinc application on millet dry matter growth, nutrition and production, grown under greenhouse conditions. The experiment was carried out in FCAV / UNESP in pots filled with a 3 dm3 sample of the superficial horizon of a medium textured Red Dystrophic Oxisol, during the period of October to December 2008. Six doses of zinc (0, 15, 30, 60, 120 and 360 mg dm-3), in the form of zinc sulphate, were applied to the soil. The experiment was arranged in a completely randomized design with four replications. 45 days after emergence, the plants were cut and height, diameter of tillers, number of tillers, leaf area and mass and Zn content in shoot dry matter were evaluated. The use of high doses of zinc decreased millet growth and dry matter production, reaching Zn the toxicity levels in the shoots of 451 mg kg-1.

Effect of Zinc Supplementation on the Status of Thyroid Hormones and Na, K, and Ca Levels in Blood Following Ethanol Feeding

The influence of zinc (Zn) on the serum levels of triiodothyronine (T(3)), thyroxine (T(4)), thyroid-stimulating hormone (TSH) and sodium (Na), potassium (K), and calcium (Ca) was evaluated following ethanol toxicity to the rats. To achieve this, male Wistar rats (150-195 g) were given 3 ml of 30% ethanol orally, and zinc was given in the form of zinc sulfate (227 mg/l) in their drinking water daily for 8 weeks. Ethanol feeding resulted in a slight decrease in T(3) and T(4) levels and a significant increase in thyroid-stimulating hormone concentration, which may be due to the direct stimulatory effect of ethanol on thyroid. Interestingly, when zinc was given to these rats, all the above levels were brought quite close to their normal levels, thus indicating the positive role of zinc in thyroid hormone metabolism. Serum Zn and Ca levels were found to be reduced, but Na levels were raised upon ethanol feeding. Restoration of normal levels of these metals upon zinc supplementation to ethanol fed rats confirms that zinc has potential in alleviating some of the altered thyroid functions following ethanol administration.

Protective Role of Zinc in Ameliorating Arsenic-Induced Oxidative Stress and Histological Changes in Rat Liver

The aim of present work was to gain insight into the role of dietary zinc in ameliorating the adverse effects caused by arsenic on rat liver. Male Wistar rats received arsenic alone in the form of sodium arsenite in drinking water at a dose level of 100 ppm, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L, or arsenic + zinc treatments in the combined group for a total duration of 3 months. Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment. Furthermore, arsenic treatment resulted in a significant decrease in hepatic zinc levels. Histological studies showed well-differentiated signs of focal hepatitis, lobular inflammation, prominent hepatocyte degeneration, and severe periportal necrosis. Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats. Further, the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment. The administration of zinc to arsenic-treated rats caused signs of improvement in liver histoarchitecture, but a few focal areas of degeneration and necrosis were still occasionally seen. In conclusion, the results of this study suggest that zinc can be beneficial against arsenic-induced hepatotoxicity in rats.

Membrane Fluidity and Surface Changes During Initiation of 1,2 Dimethylhydrazine-Induced Colon Carcinogenesis: Protection by Zinc

The present study evaluated the modulatory effects of zinc on colonic membrane fluidity and surface abnormalities following 1,2 dimethylhydrazine (DMH)-induced colon carcinogenesis. Rats were segregated into four groups: normal control, DMH treated, zinc treated, DMH + zinc treated. Colon carcinogenesis was initiated through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 8 weeks. Zinc (in the form of zinc sulphate) was supplemented to rats at a dose level of 227 mg/L in drinking water, ad libitum, for the entire duration of the study. Brush border membranes (BBM) were isolated from the colon of rats and the fluidity parameters were assessed by steady-state fluorescence polarization technique using the membrane extrinsic fluorophore 1,6-diphenyl-1,3,5-hexatriene (DPH). The translational diffusion was measured by using the excimer formation of pyrene incorporated in the membrane. The results demonstrated a significant increase in the polarization and anisotropy, accompanied by an increase in order parameter in the membrane preparations from the colon of DMH-injected rats. Further, studies with pyrene fluorophore indicated a marked decrease in membrane microviscosity following DMH treatment. However, the alterations in membrane fluorescence polarization and the fluidity parameters were completely restored following zinc treatment. Drastic alterations in colon surface were noticed after 8 weeks of DMH treatment. However, zinc treatment to DMH-treated rats greatly restored normalcy in the colonic surface. The study concludes that zinc has a strong membrane stabilizing effect and thus has a positive beneficial effect against chemically induced colonic preneoplastic progression in rats.

Role of Zinc in Modulating Histoarchitectural and Biochemical Alterations During Dimethylhydrazine (DMH)-Induced Rat Colon Carcinogenesis

The aim of the present work was to gain insight into the putative anticancer effect of dietary zinc during 1,2 dimethylhydrazine (DMH)-induced colon carcinogenesis. The rats were segregated into four groups, namely, normal control, DMH-treated, zinc-treated, and (DMH + zinc)-treated. Colon carcinogenesis was induced through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 12 weeks. Zinc in the form of zinc sulfate was supplemented to rats at a dose level of 227 mg/L in drinking water, ad libitum for the entire duration of the study. The effects of different treatments were studied on lipid peroxidation (LPO), reduced glutathione (GSH), and antioxidative enzymes, which included superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR), as well as on the histoarchitecture of the colon. A total of 12 weeks of DMH treatment resulted in a significant increase in LPO. GSH levels and the activities of SOD, CAT, and GST were found to be significantly decreased following DMH treatment. A significant elevation in the activity of GR was observed following 12 weeks of DMH treatment. Histopathological studies showed well-differentiated signs of dysplasia, which included nuclei enlargement, epithelial thickening, and nuclear pleomorphism indicative of promotional phase of colon carcinogenesis in DMH-administered rats. Administration of zinc to DMH-treated rats decreased the levels of LPO and GSH significantly, but the activities of SOD and CAT were found to be significantly increased following zinc treatment. Zinc supplementation along with DMH treatment did not reveal any significant change in the activity of GR but significantly improved the activity of GST, which was depressed following DMH treatment. Also, zinc treatment in DMH-treated rats showed signs of great improvement, but structureless masses of the cells and hyperchromic nuclei were still visible occasionally. In conclusion, the results of this study suggest that zinc has a positive beneficial effect against chemically DMH-induced colonic preneoplastic progression in rats.

Zinc improves antioxidative enzymes in red blood cells and hematology in lithium-treated rats

The present study was designed to evaluate the protective role of zinc in attenuating the adverse effects induced by lithium in blood of female Wistar rats. Female Wistar rats received lithium in the form of lithium carbonate in diet at a dose level of 1.1 g/kg diet, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L drinking water, or lithium plus zinc treatments in the combined group for a total duration of 2 months. Effects of the treatments were studied on antioxidant defense system, various hematologic parameters, and percentage of (65)Zn-specific activity. Lithium treatment resulted in a significant increase in lipid peroxidation levels but caused a significant decrease in reduced glutathione levels and the activities of catalase, glutathione S-transferase, and superoxide dismutase. Lithium treatment also caused a significant decrease in the activities of aminolevulinic acid dehydratase and Na(+) K(+) adenosine triphosphatase. However, it resulted in a significant increase in total leukocyte counts, neutrophils, and lymphocyte counts as well as zinc protoporphyrin levels, whereas a significant decrease in counts of monocytes, eosinophils, and percentage specific activity of (65)Zn in blood and its various fractions was noticed. Furthermore, lithium treatment caused a significant decrease in serum zinc levels. However, zinc supplementation to lithium-treated rats effectively raised the reduced glutathione levels and also normalized lipid peroxidation and the activities of antioxidative enzymes, which included catalase, glutathione S-transferase, and superoxide dismutase. Moreover, zinc supplementation could raise the activities of the enzymes aminolevulinic acid dehydratase and Na(+) K(+) adenosine triphosphatase as well as the percentage uptake values of (65)Zn in blood and its fractions. The study suggests that zinc, as a nutritional supplement, has the potential in attenuating most of the adverse effects induced by lithium in rat blood.

Lead-induced alterations in protein-deficient rat liver–role of zinc

This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227 mg L−1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100 mg kg−1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated PD rats. In contrast, serum AST activity was elevated both at 3 and 8 weeks while serum ALT activity was elevated at 8 weeks in Pb-treated PD rats. Pb treatment to PD rats elevated hepatic ALP, AST and ALT activities but depressed hepatic AST. Zn supplementation to Pb-treated PD rats restored the altered enzyme activities. The levels of K, Fe, Cu, Zn, Se and Rb were altered in protein deficiency. Furthermore, treatment with Pb to these animals depressed the Cu levels. Zn treatment to Pb-treated PD animals tended to restore the levels of altered elements. Hence, the present study clearly suggests that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.

Zinc mediated normalization of histoarchitecture and antioxidant status offers protection against initiation of experimental carcinogenesis

The present study evaluated the inhibitory effects of zinc on colonic antioxidant defense system and histoarchitecture during 1,2 dimethylhydrazine (DMH) induced colon carcinogenesis in male Spraque Dawley rats. The rats were segregated into four groups viz., normal control, DMH treated, zinc treated, DMH + zinc treated. Colon carcinogenesis was induced through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 8 weeks. Zinc (in the form of zinc sulphate) was supplemented to rats at a dose level of 227 mg/l in drinking water, ad libitum for the entire duration of the study. Increased lipid peroxidation was accompanied by a decrease in reduced glutathione (GSH), glutathione reductase (GR), glutathione-s-transferase (GST), superoxide dismutase (SOD), and catalase. Administration of zinc to DMH treated rats significantly decreased the lipid peroxidation levels with simultaneous enhancement of GSH, GR, GST, SOD, and Catalase. Histopathological studies from DMH treated rats revealed disorganization of colonic histoarchitecture. However, zinc treatment to DMH treated rats greatly restored normalcy in the colonic histoarchitecture, with no apparent signs of abnormality. Energy Dispersive X-Ray Fluorescence (EDXRF) studies revealed a significant decrease in tissue concentrations of zinc in the colon following DMH treatment, which upon zinc supplementation were recovered to near normal levels. In conclusion, the results of this study suggest that zinc has a beneficial effect during the initiation of key events leading to the development of experimentally induced carcinogenesis.

Effectiveness of zinc in modulating lithium induced biochemical and behavioral changes in rat brain.

1. The purpose of the present study was to determine the effect of zinc on the status of various neurotransmitters as well as behavioral patterns of lithium-treated rats. The study was designed with a view to find out whether zinc affords protection to brain against lithium toxicity. 2. Animals were segregated into four different groups. Animals in group I were fed with standard laboratory feed and water ad libitum and served as normal controls. Animals in group II and IV were given lithium in the form of lithium carbonate in their diet at a dose level of 1.1 g/Kg diet. Animals in group III and IV were given zinc treatment in the form of zinc sulfate at a dose level of 227 mg/L mixed in drinking water of animals. 3. The effects of all the treatments were studied for a duration of 1, 2, and 4 months with regard to the parameters, which included estimation of serotonin and dopamine concentrations as well as the activity of acetylcholinesterase in cerebral cortex of rat brain. Further, passive avoidance, active avoidance, and behavior despair tests were conducted to assess the short-term memory, cognitive behavior, and psychomotor dysfunction of the animals, respectively. 4. Initially, a decrease in the acetylcholinesterase activity was reported in cerebral cortex followed by an increase in the enzyme activity after 2 and 4 months of lithium treatment. Serotonin concentration significantly decreased after 2 and 4 months of lithium treatment, whereas dopamine concentration increased significantly after 4 months of lithium treatment. Zinc administration to the lithium-treated group significantly improved the acetylcholinesterase activity as well as the concentration of dopamine and serotonin. Further, lithium-treated rats showed an increase in depression time as compared to normal controls both after 1 and 4 months of treatment. Short-term memory significantly improved in lithium-treated rats in all treatment groups. However, no change in the cognitive behavior of the animals was reported after lithium treatment. Zinc co-administration with lithium significantly improved the short-term memory and cognitive functions of the animals. From the above results it can be concluded that zinc proved beneficial in altering the status of neurotransmitters as well as the behavior patters of the animals treated with both short and long-term lithium therapy.

Chemopreventive potential of zinc in experimentally induced colon carcinogenesis

The present study was performed to evaluate the efficacy of zinc treatment on colonic antioxidant defense system and histoarchitecture in 1,2-dimethylhydrazine- (DMH) induced colon carcinogenesis in male Sprague–Dawley rats. The rats were segregated into four groups viz., normal control, DMH treated, zinc treated, DMH + zinc treated. Colon carcinogenesis was induced through weekly subcutaneous injections of DMH (30 mg/kg body weight) for 16 weeks. Zinc (in the form of zinc sulphate) was supplemented to rats at a dose level of 227 mg/L in drinking water, ad libitum for the entire duration of the study. Increased tumor incidence, tumor size and number of aberrant crypt foci (ACF) were accompanied by a decrease in lipid peroxidation, glutathione- S-transferase, superoxide dismutase (SOD) and catalase. On the contrary, significantly increased levels of reduced glutathione (GSH) and glutathione reductase (GR) were observed in DMH treated rats. Administration of zinc to DMH treated rats significantly decreased the tumor incidence, tumor size and aberrant crypt foci number with simultaneous enhancement of lipid peroxidation, SOD, catalase and glutathione- S-transferase. Further, the levels of GSH and GR were also decreased following zinc supplementation to DMH treated rats. Well-differentiated signs of dysplasia were evident in colonic tissue sections by DMH administration alone. However, zinc treatment to DMH treated rats greatly restored normalcy in the colonic histoarchitecture, with no apparent signs of neoplasia. EDXRF studies revealed a significant decrease in tissue concentrations of zinc in the colon following DMH treatment, which upon zinc supplementation were recovered to near normal levels. In conclusion, the results of this study suggest that zinc has a positive beneficial effect against chemically induced colonic preneoplastic progression in rats induced by DMH.

Effectiveness of Zinc in Modulating the CCl 4 - Induced Oxidative Stress in Rat Liver

The present study was designed to evaluate the role of zinc on the enzymes involved in oxidative defense mechanism in conditions of carbon tetrachloride (CCl 4) -induced rat liver toxicity. To carry out the study, rats were divided into four groups: group I (normal control), group II (CCl 4 treated), group III (zinc control), and group IV (zinc + CCl 4 treated). Animals in group II and group IV were administered 0.1 mL of CCl 4 mixed with 0.1 mL of groundnut oil on alternate days for a period of 8 weeks. Zinc in the form of zinc sulphate was given to animals of group II and group IV at a dose level of 227 mg/L in drinking water. Animals given CCl 4 treatment alone showed a significant increase in the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and the concentration of malondialdehyde (MDA) product, whereas a significant depression was observed in the levels of reduced glutathione (GSH). Zinc treatment to CCl 4 -treated rats brought the altered levels of GSH, MDA, and SOD as observed following CCl 4 -treatment alone to within normal limits. However, the activities of catalase and glutathione peroxidase, which were increased under carbon tetrachloride treatment, were significantly attenuated and tended to become normal. Hence, the present study suggests that zinc may play an important role in regulating the activities of the enzymes involved in antioxidative defense system under CCl 4 toxic conditions.

Method of treating viscose plant wastewaters with coal wastes

Humic acids were separated from oxidized coals with a minimum yield of 50%. It was shown that sodium humate can be used for precipitating zinc from viscose plant wastewaters. Regardless of the concentration and pH of the wastewater, zinc is totally extracted from it. The zinc can be desorbed from the humate sediment in the form of zinc sulfate.

Effect of Zinc supplementation on ethanol-mediated bone alterations

Ethanol consumption leads to bone alterations, mainly osteoporosis. Ethanol itself may directly alter bone synthesis, but other factors, such as accompanying protein malnutrition—frequently observed in alcoholics-, chronic alcoholic myopathy with muscle atrophy, alcohol induced hypogonadism or hypercortisolism, or liver damage, may all contribute to altered bone metabolism. Some data suggest that zinc may exert beneficial effects on bone growth. Based on these facts, we analyzed the relative and combined effects of ethanol, protein malnutrition and treatment with zinc, 227 mg/l in the form of zinc sulphate, on bone histology, biochemical markers of bone formation (osteocalcin) and resorption (urinary hydroxyproline excretion), and hormones involved in bone homeostasis (insulin growth factor 1 (IGF-1), vitamin D, parathormone (PTH), free testosterone and corticosterone), as well as the association between these parameters and muscle fiber area and liver fibrosis, in eight groups of adult Sprague Dawley rats fed following the Lieber de Carli model during 5 weeks. Ethanol showed an independent effect on TBV ( F = 14.5, p < 0.001), causing it to decrease, whereas a low protein diet caused a reduction in osteoid area ( F = 8.9, p < 0.001). Treatment with zinc increased osteoid area ( F = 11.2, p < 0.001) and serum vitamin D levels ( F = 3.74, p = 0.057). Both ethanol ( F = 45, p < 0.001) and low protein diet ( F = 46.8, p < 0.01) decreased serum osteocalcin levels. Ethanol was the only factor independently related with serum IGF-1 ( F = 130.24, p < 0.001), and also showed a synergistic interaction with protein deficiency ( p = 0.027). In contrast, no change was observed in hydroxyproline excretion and serum PTH levels. No correlation was found between TBM and muscle atrophy, liver fibrosis, corticosterone, or free testosterone levels, but a significant relationship was observed between type II-b muscle fiber area and osteoid area ( ρ = 0.34, p < 0.01). Osteoporosis is, therefore, present in alcohol treated rats. Both alcohol and protein deficiency lead to reduced bone formation. Muscle atrophy is related to osteoid area, suggesting a role for chronic alcoholic myopathy in decreased bone mass. Treatment with zinc increases osteoid area, but has no effect on TBV.

Alcoholic myopathy: Lack of effect of zinc supplementation

A chronic form of myopathy has been described in alcoholics, characterized by atrophy of type II fibers, due both to reduced protein synthesis and increased protein breakdown. Increased production of reactive oxygen species could probably play a role in increased protein breakdown. In addition, treatment with zinc might be beneficial, since it acts as a cofactor of several enzymes involved in the synthesis of proteins and antioxidants as copper-zinc-superoxidedismutase (SOD) and selenium dependent glutathione peroxidase (GPX). Based on these facts, we analyze the relative and combined effects of ethanol, protein malnutrition and treatment with zinc, 227 mg/l in form of zinc sulphate, on muscle changes in 8 groups of adult Sprague–Dawley rats fed following the Lieber–de Carli model during 5 weeks. We also study the association between muscle histological changes and the activity of GPX, SOD and lipid peroxidation products (MDA), with hormones such as IGF-1, and with trace elements involved in antioxidant systems and/or in lipid peroxidation, such as selenium, copper, zinc, and iron. We found type IIa and IIb fiber atrophy in the alcoholic animals, especially in the low-protein fed ones. This effect was mainly due to protein deficiency. Zinc played no role at all. Muscle iron increased in ethanol, low protein fed rats, either with or without zinc, and was directly related with muscle MDA levels, which in turn were related with muscle atrophy, as was also found for serum IGF-1 levels. Ethanol was the main responsible for all these changes, although protein undernutrition also played an independent role in MDA levels. A positive interaction between ethanol and protein deficiency on serum IGF-1 was also detected. These results suggest that both protein deficiency and ethanol contribute to muscle atrophy observed in alcoholized rats; this atrophy is associated with increased lipid peroxidation and muscle iron overload. Treatment with zinc sulphate confers no benefit.