Decreased Plasma Zinc Research Articles

Zinc improved erythrocyte deformability and aggregation in patients with beta-thalassemia: An in vitro study.

Thalassemia patients have reduced red cell deformability and decreased plasma zinc levels in their blood. This study aimed to evaluate the effects of zinc (Zn) on the hemorheological parameters and antioxidant enzyme activities in β-thalassemia major (TM) and healthy volunteers (HV). Hemorheological parameters were measured using LORCA (laser-assisted optical rotational cell analyzer) after adjusting the hematocrit to 40%. Zinc sulfate (ZnSO4.7H2O) was used for Zn incubation with a concentration of 0.5μg/dl. Oxidative stress and antioxidant status were determined using commercial kits. Data showed that after Zn incubation, EImax, the area under the EI-osmolarity curve (Area), and Omax decreased in TM. However, no significant difference was observed in the osmotic deformability parameters of HV. The increased elongation index was obtained at different shear stresses for TM and HV, and SS1/2 decreased in both groups. The AMP and aggregation index (AI) decreased in TM, and the required time for half of the maximum aggregation (t1/2) increased in HV. However, Zn did not affect oxidative parameters in both groups. This study showed that Zn incubation increased deformability and decreased aggregation in thalassemic erythrocytes. It means that Zn supplementation will contribute to microcirculation in thalassemia patients.

409 Next generation sequencing-directed treatment in a patient with two co-existing genodermatoses: Acrodermatitis enteropathica (AE) and recessive dystrophic epidermolysis bullosa (RDEB)

Next generation sequencing (NGS) is helpful in diagnosing complex genetic phenotypes. Here we report a case with two co-existing heritable skin diseases. The proband, a 17-year-old female, born to consanguineous parents, demonstrated widespread refractory erythematous and desquamative plaques, generalized alopecia, and growth failure. She was clinically diagnosed with RDEB, based on the history of neonatal blistering, recurrent oral blisters and esophageal involvement. This diagnosis was confirmed by whole exome sequencing (WES) demonstrating a homozygous mutation, c.5820G>A, in COL7A1, and supported by aberrant expression of type VII collagen and reduced anchoring fibrils. This synonymous mutation replaces the last nucleotide of exon 70, and RNA-seq revealed aberrant splicing, including exclusion of exon 70 and retention of intron 70 sequences. The laboratory findings included decreased plasma zinc level [40 mg/dL, normal range 70-150 mg/dL], which was thought to be a sequela of EB-associated malabsorption. However, daily supplementation of diet with zinc at 1 mg/kg/per day did not alter the clinical presentation. Careful examination of the genomic database from WES revealed the presence of a homozygous missense mutation, c.653C>G; p.Pro218Arg, in SLC39A4, gene associated with zinc deficiency in AE. Now, increasing the supplementation of zinc to 3 mg/kg/per day resulted in rapid and dramatic resolution of the skin findings, with subsequent growth and weight gain. This case demonstrates the power of NGS in identifying two genetically unlinked diseases that led to effective treatment with major clinical benefits.

Plasma zinc in institutionalized elderly individuals: Relation with immune and cardiometabolic biomarkers

Changes in zinc metabolism caused by aging and the institutionalization process may contribute to zinc deficiency in elderly individuals. Hypozincemia results in changes in glycemic, lipid, and inflammatory profiles. The aim of this study was to evaluate plasma zinc concentrations and their relationships with sociodemographic, dietary, inflammatory, and cardiometabolic biomarkers in institutionalized elderly individuals. A cross-sectional study was carried out including 255 elderly adults living in nursing homes. The associations between plasma zinc and dietary zinc intake, sociodemographic indicators, and glycemic, lipid, and inflammatory biomarkers were evaluated. Independent variables were analyzed according to quartiles of plasma zinc concentrations (Q1: <71.1 μg/dL; Q2: 71.1–83.3 μg/dL; Q3: <83.3–93.7 μg/dL; Q4: >93.7 μg/dL). The relationship between plasma zinc concentrations and predictor variables was also tested. In Q1, higher concentrations of the following variables were observed, compared with those in other quartiles: total cholesterol and low-density lipoprotein cholesterol (LDL-c; Q1 > Q2, Q3, Q4; all p <0.001); triglycerides (Q1 > Q3, Q4; all p < 0.001); interleukin (IL)-6 (Q1 > Q3, Q4; p = 0.024 and p = 0.010, respectively); tumor necrosis factor (TNF)-α (Q1 > Q3, p = 0.003). A significant reduction in plasma zinc concentrations was observed with increasing age-adjusted institutionalization time (Δ = − 0.10; 95% confidence interval [CI]: −0.18 to −0.01). The concentrations of total cholesterol (Δ = − 0.19; 95% CI: −0.23 to −0.15), LDL-c (Δ = − 0.19; 95% CI: −0.23 to −0.15), triglycerides (Δ = − 0.11; 95% CI: −0.16 to −0.06), IL-6 (Δ = − 1.41; 95% CI: −2.64 to −0.18), and TNF-α (Δ = − 1.04; 95% CI: −1.71 to −0.36) were also significantly increased. In conclusion, decreased plasma zinc concentrations were associated with longer institutionalization time and worse lipid and inflammatory profiles in elderly institutionalized individuals.

Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper

Zinc and copper are essential trace elements. Dyshomeostasis in these two metals has been observed in Alzheimer’s disease, which causes profound cognitive impairment. Insulin therapy has been shown to enhance cognitive performance; however, recent data suggest that this effect may be at least in part due to the inclusion of zinc in the insulin formulation used. Zinc plays a key role in regulation of neuronal glutamate signaling, suggesting a possible link between zinc and memory processes. Consistent with this, zinc deficiency causes cognitive impairments in children. The effect of zinc supplementation on short- and long-term recognition memory, and on spatial working memory, was explored in young and adult male Sprague Dawley rats. After behavioral testing, hippocampal and plasma zinc and copper were measured. Age increased hippocampal zinc and copper, as well as plasma copper, and decreased plasma zinc. An interaction between age and treatment affecting plasma copper was also found, with zinc supplementation reversing elevated plasma copper concentration in adult rats. Zinc supplementation enhanced cognitive performance across tasks. These data support zinc as a plausible therapeutic intervention to ameliorate cognitive impairment in disorders characterized by alterations in zinc and copper, such as Alzheimer’s disease.

Protein Malnutrition During Juvenile Age Increases Ileal and Colonic Permeability in Rats.

Protein malnutrition can lead to morphological and functional changes in jejunum and ileum, affecting permeability to luminal contents. Regarding the large intestine, data are scarce, especially at juvenile age. We investigated whether low-protein (LP) diet could modify ileal and colonic permeability and epithelial morphology in young rats. Isocaloric diets containing 26% (control diet) or 4% protein were given to male rats between postnatal days 40 and 60. LP-diet animals failed to gain weight and displayed decreased plasma zinc levels (a marker of micronutrient deficiency). In addition, transepithelial electrical resistance and occludin expression were reduced in their ileum and colon, indicating increased gut permeability. Macromolecule transit was not modified. Finally, LP diet induced shortening of colonic crypts without affecting muscle thickness. These data show that protein malnutrition increases not only ileum but also colon permeability in juvenile rats. Enhanced exposure to colonic luminal entities may be an additional component in the pathophysiology of protein malnutrition.

Zinc and Zinc Related Enzymes in Precancerous and Cancerous Tissue in the Colon of Dimethyl Hydrazine Treated Rats

Trace element zinc deficiency or excess is implicated in the development or progression of some cancers. The exact role of zinc in the etiology of colon cancer is unclear. To cast light on this question, an experimental model of colon carcinogenesis was applied here. Six week old rats were given sub cutaneous injections of DMH (30 mg/kg body weight) twice a week for three months and sacrificed after 4 months (precancer model) and 6 months (cancer model). Plasma zinc levels showed a significant decrease (p<0.05) at 4 months and a greater significant decrease at 6 months (p<0.01) as compared with controls. In the large intestine there was a significant decrease in tissue zinc levels (p<0.005) and in CuZnSOD, and alkaline phosphatase activity (p<0.05) in the pre-cancerous model and a greater significant decrease in tissue zinc (p<0.0001), and in CuZnSOD and alkaline phosphatase activity (p<0.001), in the carcinoma model. The tissue zinc levels showed a significant decrease in the small intestine and stomach (p<0.005) and in liver (p<0.05) in the cancer model. 87% of the rats in the precancer group and 92% rats in the cancer group showed histological evidence of precancerous lesions and carcinomas respectively in the colon mucosa. This study suggests that the decrease in plasma zinc, tissue zinc and activity of zinc related enzymes are associated with the development of preneoplastic lesions and these biochemical parameters further decrease with progression to carcinoma in the colon.

Effects of intravenous Escherichia coli dose on the pathophysiological response of colostrum-fed Jersey calves

Objectives of the present study were to characterize the dose dependency of an intravenous Escherichia coli O111:H8 challenge in colostrum-fed Jersey calves and to identify any biochemical markers indicative of septicemia. Eighteen 3-week old colostrum-fed Jersey calves were completely randomized to 1 of 6 doses of E. coli O111:H8. The challenge doses included 0, 1.5 × 10 5, 1.5 × 10 6, 1.5 × 10 7, 1.5 × 10 8, and 1.5 × 10 9 colony-forming units (CFU) given intravenously as a bolus in 5 mL of sterile isotonic saline. Peripheral blood samples were collected at 0, 2, 4, 8, 12, 24, and 48 h relative to the challenge for biochemical, total leukocyte count, and differential analyses. Rectal temperatures were collected via indwelling rectal temperature probes at 5-min intervals, and hourly averages calculated from 2 d prior to the challenge till 2 d after the challenge. All calves survived the 48 h observation period following the challenge. Calves given 1.5 × 10 8 and 1.5 × 10 9 CFU displayed sickness behaviors ( P < 0.01) beginning 0.5 h after the challenge and returned to that of the control calves by 6 and 32 h for calves challenged with 1.5 × 10 8 and 1.5 × 10 9 CFU, respectively. There were treatment × time interactions ( P < 0.01) on total leukocyte counts and plasma glucose and zinc concentrations. Calves administered 1.5 × 10 8 and 1.5 × 10 9 CFU had leucopenia beginning 2 h after the challenge and returning to counts similar to the control calves within 24 h. Additionally, those calves were hypoglycemic from 4 to 12 h after the challenge with the degree of hypoglycemia inversely related to the dose of the E. coli. All calves challenged with E. coli had decreased plasma zinc concentrations, and the magnitude was inversely proportional to the challenge dose. There were treatment × time interactions ( P < 0.001) on rectal temperatures following the challenge. All calves challenged with E. coli developed a febrile response, but the intensity and duration of the response were dependent on the challenge dose. These data indicate that calves intravenously challenged with 1.5 × 10 8 and 1.5 × 10 9 CFU of the E. coli O111:H8 showed immediate clinical and biochemical signs indicative of septicemia. However, calves administered 1.5 × 10 7 or less of the E. coli had febrile responses, but did not develop septicemia. Blood glucose and zinc concentrations may be dose responsive indicators that could potentially differentiate between a septicemic versus non-septicemic calf.

Different Recovery Responses from Dietary Zinc-Deficiency in the Distribution of Rat Granulocytes

The purpose of this study was to elucidate the effects of the recovery from dietary zinc-deficiency on the number of total white blood cells (WBCs), neutrophils, eosinophils and basophils, and plasma zinc and corticosterone concentrations in weanling male Sprague Dawley rats. Rats (n=34) of the zinc-deficient diet (0.6 mg zinc/kg diet) and control diet (35.2 mg zinc/kg diet) groups were fed for 4 wk, and then rats of both groups were fed with the control diet for 3 wk. Zinc-deficiency increased duration-dependently and clearly the number of total WBCs, neutrophils and eosinophils, and the increased numbers of these cells recovered to the control levels in week 2 of the recovery. On the other hand, the number of basophils increased by the zinc-deficiency recovered to the control levels in week 1 of the recovery. Zinc-deficiency significantly decreased plasma zinc concentrations by 85%, and markedly increased plasma corticosterone concentrations by 317%, as compared with the control group. In the recovery period, plasma zinc and corticosterone concentrations recovered to the control levels in week 2 of the recovery. These results suggest that zinc-deficiency and its recovery responses in the number of granulocytes and total WBCs are reversible, and their recovery rates depend on the subsets of granulocytes in rats.

Iron chelation therapy for patients with sickle cell disease and iron overload

A 21-year-old male with sickle cell disease (SCD) presented with severe pallor. He had received a total of 100 red blood cell (RBC) units in his lifetime, had a mean serum ferritin level of 3133 ng/ml, and liver iron concentration (LIC) of 12 mg Fe/g dry weight (dw). He was started on subcutaneous deferoxamine (DFO) infusions at a dose of 56 mg/kg/d, five days a week (equivalent to 40 mg/kg/d, seven days a week) and continued to receive 8–10 RBC units/year as treatment for pain. During the first six months of chelation therapy, his serum ferritin levels fell by around 50% of the pretreatment value, but then started to increase back up to the baseline values. The patient was noncompliant with DFO therapy. He experienced pain at the site of injection, could not sleep and was concerned about carrying a pump and not being accepted by his peers. He dropped out of college and abstained from all social activities. He was referred to a psychologist; however, this failed to improve compliance and he opted to stop DFO therapy altogether.

Association of MT1A haplotype with cardiovascular disease and antioxidant enzyme defense in elderly Greek population: comparison with an Italian cohort

Metallothioneins (MT), the antioxidant zinc-binding proteins, seem to mediate cardioprotection. It has been postulated that zinc homeostasis and MT function may be altered, as a consequence of oxidative stress, in cardiovascular disease (CVD), with a potential implication of MT genetic polymorphisms. The present study explores the role of +647A/C and +1245A/G MT1A polymorphisms on the susceptibility to CVD, zinc status and enzyme antioxidant activity, in the Greek and Italian populations. The country selection was based on the lower zinc status and the reduced zinc dietary intake in Greece than in Italy despite the similar Mediterranean dietary pattern. A total of 464 old, healthy control subjects and 369 old CVD patients more than 70 years of age were studied. Logistic regression model indicated that +1245 MT1A G+ genotype significantly increased the risk of CVD in Greece (34.4% vs. 23.2%; odds ratio=1.88, 95% confidence interval=1.14–3.08; P=.013) but not in Italy. Haplotype analysis showed an increment of CG haplotype frequency in CVD Greek patients (17.4% vs. 10.6%, P<.05). Differential country-related frequency distribution was also recorded. Applying a multivariate regression model, +647/+1245 MT1A haplotype was associated with a modulation of enzyme antioxidant activities in both countries. Decreased plasma zinc and reduced intracellular Zn release, as well as increased enzyme antioxidant activity, were more apparent in Greek healthy donors than in Italy. In conclusion, +1245 MT1A polymorphism and +647/+1245 MT1A haplotype are implicated in CVD in Greece but not in Italy, suggesting a role of gene–diet interaction in the disease predisposition.

Tissue zinc levels in precancerous tissue in the gastrointestinal tract of azoxymethane (AOM)-treated rats

Alterations in tissue zinc levels have been documented in patients with gastrointestinal tract malignancies and more frequently, in those with colonic cancer. However, the precise role of tissue zinc in carcinogenesis is not well elucidated. This study, using a well-established colon cancer model in rats, was designed to investigate the relationship of tissue zinc to the carcinogenic process. The aim was to examine tissue zinc levels in the preneoplastic tissues and to study the changes that occur during transition of mucosa from normal to preneoplastic state. Six-week old rats were given a single dose subcutaneous injection of azoxymethane (AOM) (30 mg/kg body weight) and sacrificed after 1, 2, 5, and 9 months of the treatment. Plasma zinc levels showed a significant decrease ( p<0.05) at 9 months compared with controls. Tissue zinc levels showed a significant decrease in the large intestine at 1 and 2 months ( p<0.05) and at 5 and 9 months ( p<0.01), in the small intestine at 2, 5, and 9 months ( p<0.05), and in the stomach at 5 and 9 months ( p<0.05). The maximum percent decrease (45%) in tissue zinc was observed in the large intestine at 9 months. Tissue copper zinc super oxide dismutase (CuZnSOD) activity was assessed in the body of the stomach, small intestine, and large intestine and compared with the control group. There was a significant fall in CuZnSOD levels in the small intestine at 9 months ( p<0.05) and in the large intestine at 5 and 9 months ( p<0.01). Two of these six rats showed histological evidence of precancerous lesions in the mucosa of the colon. This study suggests that the decrease in plasma zinc, tissue zinc and activity of CuZnSOD is associated with development of preneoplastic lesions in the colonic mucosa.

Clinical, immunological, anti-inflammatory and antioxidant roles of zinc

The essentiality of zinc for humans was recognized only 40 years ago. Zinc deficiency was suspected to occur in Iranian patients with growth retardation, hypogonadism in males, hepato-splenomegaly, rough and dry skin, geophagia and severe iron deficiency anemia. Later we documented zinc deficiency in similar patients in Egypt. The diet of these patients consisted of mainly cereal proteins which contained high phytate and this led to decreased availability of iron and zinc. These patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, decreased serum thymulin activity hyperammonemia, neuro-sensory disorders and decreased lean body mass.The basic mechanisms of zinc action on immune cells have been reviewed in this paper. Our studies showed that the activation of many zinc dependent enzymes and transcription factors were affected adversely due to zinc deficiency. The gene expression and production of Th1 cytokines were affected adversely due to zinc deficiency.Zinc is also an antioxidant and has anti-inflammatory actions. We have reported decreased plasma zinc, increased plasma oxidative stress markers and increased generation of inflammatory cytokines in the elderly subjects which were corrected by zinc supplementation. In cell culture studies, we have observed that zinc induces A20 which inhibits NF-κB activation resulting in decreased generation of inflammatory cytokines.

Amyloid plaques arise from zinc-enriched cortical layers in APP/PS1 transgenic mice and are paradoxically enlarged with dietary zinc deficiency

The ZnT3 zinc transporter is uniquely expressed in cortical glutamatergic synapses where it organizes zinc release into the synaptic cleft and mediates β-amyloid deposition in transgenic mice. We studied the association of zinc in plaques in relation to cytoarchitectural zinc localization in the APP/PS1 transgenic mouse model of Alzheimer’s disease. The effects of low dietary zinc for 3 months upon brain pathology were also studied. We determined that synaptic zinc distribution within cortical layers is paralleled by amyloid burden, which is heaviest for both in layers 2–3 and 5. ZnT3 immunoreactivity is prominent in dystrophic neurites within amyloid plaques. Low dietary zinc caused a significant 25% increase in total plaque volume in Alzheimer’s mice using stereological measures. The level of oxidized proteins in brain tissue did not changed in animals on a zinc-deficient diet compared with controls. No obvious changes were observed in the autometallographic pattern of zinc-enriched terminals in the neocortex or in the expression levels of zinc transporters, zinc importers or metallothioneins. A small decrease in plasma zinc induced by the low-zinc diet was consistent with the subclinical zinc deficiency that is common in older human populations. While the mechanism remains uncertain, our findings indicate that subclinical zinc deficiency may be a risk factor for Alzheimer’s pathology.

Aşı Uygulamasının Oluşturduğu Stresin Kan Plazması Bakır, Çinko, Potasyum ve Magnezyum Değerleri Üzerine Etkisi

The objective of this investigation was to reveal plasma copper, zinc, potassium, and magnesium levels of cattle under the stress of food and mouth diseases vaccination. Six female and one male cattle aged three years old were used for this investigation. As a result of this investigation, a decrease in plasma zinc and magnesium levels (P 0.05) were observed after the vaccination.

Zinc Level of Major Thalasemics in Kermanshah

Introduction: Zinc has a significant positive effect on the immune system and physical development in human beings. Many investigators believe that the level of plasma zinc in thalasemic patients is reduced firstly because of receiving chelators like desferoxamin, and secondly because of impairment of some organs like kidney, liver, thyroid and hypophysis. Therefore this study was carried out to determine the level of plasma zinc in major thalasemics referred to the Thalasemic Centre of Kermanshah during 2002. Materials & Methods: This study was a descriptive study in which 100 major thalasemics were investigated. First of all some criteria with a checklist including age, weight, and sex were collected to know how many desferalls and packs of blood they received. Plasma zinc level was determined using the flam photometer atomic absorption method. Serum ferritin level was measured using radio immuno assay and blood urea and creatinin using auto analyzer method. ANOVA and Chi square test were used for statistical analysis. Results: The mean of the patients age was 10.46± 5.25 yr, 53% was male and 47% female. Most of them had a normal level of zinc and also 23% of them had a high level of zinc. 80% of patients received packs of blood more than 240 ml/kg/yr and the correlation between plasma zinc and blood transfusion in them was statistically significant (P= 0.025). Patients who received transfusion more than normal present much higher hevel of zinc than patients received an abnormal level of desferoxamin. The study showed that correlation between plasma zinc and blood urea was statistically significant (p=0.009). Conclusion: This study showed that there was no decrease in plasma zinc of the patients. The findings showed that their treatment based on desferoxamin and transfusion has not been closely regulated and this may significantly affect the zinc status. Therefore decision on the requirement of zinc in such patients needs further studies. With satisfactory well-controlled treatment in these patients it is recommended that the level of zinc in such patients be determined by not only in plasma but also in 24 hours urine sample collections.

Perinatal ω-3 polyunsaturated fatty acid supply modifies brain zinc homeostasis during adulthood

Dietary omega-3 polyunsaturated fatty acid (PUFA) influences the expression of a number of genes in the brain. Zinc transporter (ZnT) 3 has been identified as a putative transporter of zinc into synaptic vesicles of neurons and is found in brain areas such as hippocampus and cortex. Neuronal zinc is involved in the formation of amyloid plaques, a major characteristic of Alzheimer's disease. The present study evaluated the influence of dietary omega-3 PUFA on the expression of the ZnT3 gene in the brains of adult male Sprague-Dawley rats. The rats were raised and/or maintained on a control (CON) diet that contained omega-3 PUFA or a diet deficient (DEF) in omega-3 PUFA. ZnT3 gene expression was analyzed by using real-time PCR, free zinc in brain tissue was determined by zinquin staining, and total zinc concentrations in plasma and cerebrospinal fluid were determined by atomic absorption spectrophotometry. Compared with CON-raised animals, DEF-raised animals had increased expression of ZnT3 in the brain that was associated with an increased level of free zinc in the hippocampus. In addition, compared with CON-raised animals, DEF-raised animals had decreased plasma zinc level. No difference in cerebrospinal fluid zinc level was observed. The results suggest that overexpression of ZnT3 due to a perinatal omega-3 PUFA deficiency caused abnormal zinc metabolism in the brain. Conceivably, the influence of dietary omega-3 PUFA on brain zinc metabolism could explain the observation made in population studies that the consumption of fish is associated with a reduced risk of dementia and Alzheimer's disease.

Acrodermatite entéropathique chez un nourrisson né à terme nourri exclusivement au sein

Acrodermatitis enteropathica is a rare autosomal recessive disorder, caused by impaired absorption of zinc from the gastrointestinal tract. Symptoms of acrodermatitis enteropathica occur within the first few months after birth and tend to appear shortly after discontinuation of breast-feeding. We report a breast-fed infant with acrodermatitis enteropathica. A full term, 4-month-old girl, consulted in dermatologic department for persistent and refractory anogenital lesions since the age of 1 month, with progressive erythematous, vesiculous and squamous lesions, sometimes erosive in a peri orificial and acral pattern. She was calm and healthy baby. She was breast feeding. The diagnosis of acrodermatitis enteropathica was confirmed by decreased plasma zinc level (14 microg/100 ml). Breast milk zinc levels was low (46 microg/100 ml), as plasma zinc level of the mother (94 microg/100 ml). A genetic study showed that she was homozygous for the mutation, whereas her brother and parents were heterozygous. She was given zinc sulphate, and her condition has improved significantly. Acrodermatitis enteropathica is characterized by a characteristic clinical feature and the diagnosis is confirmed by decreased plasma zinc level. Acrodermatitis enteropathica in exclusively breast fed infant is rare, it was essentially reported in premature babies. Our case report is particular because it's concerning a full-term breast-fed infant, with zinc deficiency in breast milk and mother's decreased plasma zinc level.

Plasma Lipid Peroxidation Zinc And Erythrocyte Cu-Zn Superoxide Dismutase Enzyme Activity In Patients With Type 2 Diabetes Mellitus In Gorgan City (South East Of The Caspian Sea)

The aim of this study was to determine the changes of plasma lipid peroxidation, zinc and erythrocyte Cu-Zn superoxide dismutase activity in patients with type 2 diabetes mellitus and healthy control in Gorgan city. Fifty type 2 patients with diabetes mellitus and 50 people without diabetes were included in this randomized study. None of patients studied had any diabetic complications. The levels of plasma malondialdehyde and zinc from type 2 diabetes mellitus patients (6.24±0.85 nmol mL-1 and 116.78±5.51 μ dL-1) and control groups (3.63±0.97 nmol mL-1 and 146.86±9.06 μg dL-1) were determined. Erythrocyte Cu-Zn superoxide dismutase activity from patients with diabetes (675.34±60.89 U g-1 Hb) and control groups (1052.70± 52.76 U g-1 Hb) were determined. The increased plasma lipid peroxidation and decreased plasma zinc and erythrocyte Cu-Zn superoxide dismutase activity that we observed in patients with type 2 diabetes mellitus may predispose to the development of cardiovascular complications. We propose that diabetic patients may have elevated requirement for antioxidants. Supplementation with zinc and vitamin or dietary free radical scavengers such as vitamins E and C or tomato, orange and etc. have a potential role in boosting antioxidant-related defences and maybe important in patients with diabetes.

Predictors of plasma zinc concentrations in children with acute diarrhea

Plasma and serum zinc concentrations are the most widely used markers of zinc status in individual persons and populations. The objective was to identify factors that influence plasma zinc concentrations during acute childhood diarrhea. This was a cross-sectional study of 1757 cases of acute diarrhea in 6-35-mo-old Nepalese children. The association between plasma zinc concentration and several clinical, anthropometric, socioeconomic, and biochemical variables was estimated in simple and multiple linear regression analyses. We observed a reduction in the mean plasma zinc concentration of 0.59 (95% CI: 0.44, 0.74) micro mol/L per degree ( degrees C) increase in axillary temperature. Having dysentery and an elevated plasma C-reactive protein concentration was also independently associated with lower plasma zinc. Children with clinical features of dehydration had higher plasma zinc concentrations than did those who were not dehydrated. Furthermore, a decrease in plasma albumin of 1 g/L was associated with a decrease in plasma zinc of 0.25 (95% CI: 0.21, 0.29) micro mol/L. The plasma albumin concentration confounded the associations between some clinical variables and plasma zinc, but the association between axillary temperature and dehydration on one hand and plasma zinc on the other was not substantially influenced by the albumin concentration. Moreover, the plasma zinc concentration increased with an increase in observed hemolysis. Dehydration, clinical and biochemical indicators of inflammation and hemolysis, and, when possible, plasma albumin concentrations should be taken into account when the plasma zinc concentration is used to estimate zinc status during episodes of diarrhea in childhood.

Liver and Renal Function Tests in Artisans Occupationally Exposed to Lead in Mechanic Village in Nnewi, Nigeria

Additives in petroleum solvents have been reported to have adverse health implications. An evaluation study on some toxicological effects of occupational exposure to petroleum products (especially petrol which contains tetraethyl lead) amongst twenty five occupationally exposed artisans and twenty five graduate students of College of Health Sciences, Nnamdi Azikiwe University, Nnewi, Nigeria as controls, was carried out using the following biochemical markers: electrolytes, urea, uric acid, inorganic phosphorus, creatinine, zinc and blood lead, as well as the activities of alanine and aspartate aminotransferases, and alkaline phosphatase. The results showed that occupational exposure of human subjects to lead in petrol increases the concentrations of uric acid (357 +/- 123micro mol/L) and phosphate (1.5 +/- 0.5m mol/L) in exposed subjects compared with unexposed subjects (uric acid 228 +/- 105micro mol/L, phosphate 1.2 +/- 0.41m mol/L; p < 0.01 in both cases). Significantly lower activities were observed for alkaline phosphatase (66 +/- 18.9 iu/L). The activities of alanine aminotransferase (11.4 +/- 4.0 iu/L) and aspartate aminotransferase (15.8 +/- 4.4 iu/L) in occupationally exposed artisans were higher compared with unexposed subjects (alkaline phosphatase = 78 +/- 22.4 iu/L alanine aminotranferase = 6.8 +/- 2.7 iu/L, aspartate aminotranferase = 9.6 +/- 3.5i u+/-L; p < 0.01 in all cases). Occupational exposure of human subjects to lead significantly increased blood lead (59.6 +/- 15.9 microg/dL) and decreased plasma zinc (71.3 +/- 14.4 microg/L) in exposed compared with unexposed subjects (blood lead = 35 +/- 7 microg/dL, zinc = 108.4 +/- 16.9 microg/dL; p < 0.01). The results indicate that occupational exposure to lead in petrol may compromise liver and renal function.