Percentage Of Methemoglobin Research Articles

The stability of blood gases and CO-oximetry under slushed ice and room temperature conditions.

Human blood gas stability data is limited to small sample sizes and questionable statistical techniques. We sought to determine the stability of blood gases under room temperature and slushed iced conditions in patients using survival analyses. Whole blood samples from ∼200 patients were stored in plastic syringes and kept at room temperature (22-24°C) or in slushed ice (0.1-0.2°C) before analysis. Arterial and venous pO2 (15-150mmHg), pCO2 (16-72mmHg), pH (6.73-7.52), and the CO-oximetry panel [total hemoglobin (5.4-19.3g/dL), percentages of oxyhemoglobin (O2Hb%, 20-99%), carboxyhemoglobin (COHb, 0.1-5.4%) and methemoglobin (MetHb, 0.2-4.6%)], were measured over 5-time points. The Royal College of Pathologists of Australasia's (RCPA's) criteria determined analyte instability. Survival analyses identified storage times at which 5% of the samples for various analytes became unstable. COHb and MetHb were stable up to 3h in slushed ice and at room temperature; pCO2, pH was stable at room temperature for about 60min and 3h in slushed ice. Slushed ice shortened the storage time before pO2 became unstable (from 40 to 20min), and the instability increased when baseline pO2 was≥60mmHg. The storage time for pO2, pCO2, pH, and CO-oximetry, when measured together, were limited by the pO2. When assessing pO2 in plastic syringes, samples kept in slushed ice harm their stability. For simplicity's sake, the data support storage times for blood gas and CO-oximetry panels of up to 40min at room temperature if following RCPA guidelines.

Alpha-Lipoic Acid and Its Enantiomers Prevent Methemoglobin Formation and DNA Damage Induced by Dapsone Hydroxylamine: Molecular Mechanism and Antioxidant Action

Dapsone (DDS) therapy can frequently lead to hematological side effects, such as methemoglobinemia and DNA damage. In this study, we aim to evaluate the protective effect of racemic alpha lipoic acid (ALA) and its enantiomers on methemoglobin induction. The pre- and post-treatment of erythrocytes with ALA, ALA isomers, or MB (methylene blue), and treatment with DDS-NOH (apsone hydroxylamine) was performed to assess the protective and inhibiting effect on methemoglobin (MetHb) formation. Methemoglobin percentage and DNA damage caused by dapsone and its metabolites were also determined by the comet assay. We also evaluated oxidative parameters such as SOD, GSH, TEAC (Trolox equivalent antioxidant capacity) and MDA (malondialdehyde). In pretreatment, ALA showed the best protector effect in 2.5 µg/mL of DDS-NOH. ALA (1000 µM) was able to inhibit the induced MetHb formation even at the highest concentrations of DDS-NOH. All ALA tested concentrations (100 and 1000 µM) were able to inhibit ROS and CAT activity, and induced increases in GSH production. ALA also showed an effect on DNA damage induced by DDS-NOH (2.5 µg/mL). Both isomers were able to inhibit MetHb formation and the S-ALA was able to elevate GSH levels by stimulating the production of this antioxidant. In post-treatment with the R-ALA, this enantiomer inhibited MetHb formation and increased GSH levels. The pretreatment with R-ALA or S-ALA prevented the increase in SOD and decrease in TEAC, while R-ALA decreased the levels of MDA; and this pretreatment with R-ALA or S-ALA showed the effect of ALA enantiomers on DNA damage. These data show that ALA can be used in future therapies in patients who use dapsone chronically, including leprosy patients.

Transcutaneous monitoring of hemoglobin derivatives during methemoglobinemia in rats using spectral diffuse reflectance.

.Significance: Untreated methemoglobinemia may cause severe hypoxemia and even death when methemoglobin levels in the blood stream exceed 70%. Although CO-oximetry can be used to monitor the response to treatment for methemoglobinemia, it is costly and requires an invasive procedure for collecting blood samples from patients. A pulse CO-oximeter with a contact probe can be used to continuously and non-invasively measure the percentage of methemoglobin, as well as the percutaneous oxygen saturation. In terms of the prevention of infectious diseases, however, it is desirable to monitor methemoglobin and oxygen saturation levels in a non-contact manner. Diffuse reflectance spectral imaging is promising as a non-contact, non-invasive, and cost-effective clinical diagnostic tool for methemoglobinemia.Aim: To demonstrate the feasibility of visible spectral diffuse reflectance for in vivo monitoring of hemoglobin derivatives and evaluating methemoglobin production and reduction as well as hypoxemia during methemoglobinemia in rats.Approach: A new imaging approach based on the multiple regression analysis aided by Monte Carlo simulations for light transport was developed to quantify methemoglobin, oxygenated hemoglobin, and deoxygenated hemoglobin using a hyperspectral imaging system. An in vivo experiment with rats exposed to sodium nitrite () at different doses was performed to confirm the feasibility of the method for evaluating the dynamics of methemoglobin, oxygenated hemoglobin, and deoxygenated hemoglobin during methemoglobinemia. Systemic physiological parameters, including the percutaneous arterial oxygen saturation, heart rate (HR), and pulse distention, were measured by a commercially available pulse oximeter, and the results were compared to those obtained by the proposed method.Results: Both the methemoglobin concentration and methemoglobin saturation rapidly increased with a half-maximum time of . They reached their maximal values nearly 60 min after the administration of . Tissue oxygen saturation dramatically dropped to a minimum of , , , and on average for doses of 25, 37.5, 50, and 75 mg/kg, respectively. Changes in methemoglobin concentration and tissue oxygen saturation are indicative of the temporary production of methemoglobin and severe hypoxemia during methemoglobinemia. Profound increases in the HR and pulse distention implied an elevated cardiac output caused by tachycardia and the resultant increase in peripheral blood volume to compensate for the hypoxia and hypoxemia during methemoglobinemia. This was in agreement with the time course of the peripheral hemoglobin volume concentration obtained by the proposed method.Conclusions: The proposed method is capable of the in vivo non-contact simultaneous evaluation of methemoglobin levels and hypoxemia during methemoglobinemia, and that it has potential as a tool for the diagnosis and management of methemoglobinemia.

FOXE1 polymorphisms and chronic exposure to nitrates in drinking water cause metabolic dysfunction, thyroid abnormalities, and genotoxic damage in women.

Nitrates in drinking water has been associated to adverse health effects, including changes in glucose and lipid levels, thyroid hormone imbalance and adverse reproductive effects. We analyzed metabolic and thyroid hormone alterations and genotoxic damage in women with chronic exposure to nitrates in drinking water. The concentration of nitrates in drinking water was quantified and according to this parameter, participants were divided into three exposure scenarios. Blood and urine samples were collected from 420 women living in Durango, Mexico and biomarkers were determined. We found nitrates concentrations in drinking water above the permissible limit (>50 mg/L), and an increase in the percentage of methemoglobin (p=0.0001), nitrite in blood plasma and urine (p=0.0001), glucose (p=0.0001), total cholesterol (p=0.001), LDL (p=0.001) and triglycerides (p=0.0001). We also found alterations in TSH (p=0.01), fT3 (p=0.0003), T4T (p=0.01) and fT4 (p=0.0004) hormones. Frequency of subclinical hypothyroidism was 8.33%; differences in FOXE1 (rs965513, rs1867277) genotypes distribution were found and both polymorphisms were associated with a decrease in TSH. A high percentage of micronucleus in binucleate lymphocyte cells was found (35%, p=0.0001). In conclusion, the chronic exposure to nitrates in water for human consumption caused metabolic and hormonal alterations and genotoxic damage in women.

Methemoglobin concentrations in three salmonid species following exposure to benzocaine or tricaine methanesulfonate.

Methemoglobin is hemoglobin containing ferric iron rather than ferrous iron which renders it incapable of binding to oxygen. Blood sampling of fish is done under sedation or general anesthesia. Tricaine methanesulfonate (TMS) or benzocaine is commonly used but both can cause oxidation of hemoglobin to methemoglobin. Our objective was to determine if methemoglobin concentrations in healthy rainbow trout (Oncorhynchus mykiss), brook trout (Salvelinus fontinalis), or Atlantic salmon (Salmo salar) increase during sedation with 25mg/L of a 10% benzocaine solution or with repeated short anesthetizations by 65mg/L of 10% benzocaine solution or 65mg/L of TMS. Sedation by benzocaine caused a significant increase in methemoglobin in all species over time (P <0.05). The methemoglobin percentage in brook trout increased by 129%, rainbow trout by 42%, and Atlantic salmon by 49%. The methemoglobin in brook trout was significantly greater than the other species at multiple time points. Repeated brief anesthetizing by benzocaine and TMS caused significant methemoglobin by 60 (P <0.05), 90 (P <0.01), and 120min (P <0.001) in brook trout but no significant change in methemoglobin in rainbow trout or Atlantic salmon except at 120min in Atlantic salmon (P < 0.05) repeatedly anesthetized with benzocaine. For example, following multiple anesthetizations with benzocaine, the methemoglobin percentage in brook trout increased by 140%, whereas the rise in methemoglobin in rainbow trout and Atlantic salmon was more modest (37% increase in Rainbow trout and 53% increase in Atlantic salmon). Following multiple anesthetizations with TMS, the methemoglobin increased by 90%, 5%, and 1% in brook trout, rainbow trout, and Atlantic salmon, respectively. Methemoglobin may increase significantly over time in fish immersed in a sedating dose of benzocaine or repeatedly anesthetized with benzocaine or TMS. The susceptibility varies with the individual and species with brook trout being more susceptible than Atlantic salmon or rainbow trout.

27-Year-Old Woman With Fever, Headache, and Anemia

27-Year-Old Woman With Fever, Headache, and Anemia

Fluorescent Heme Degradation Products Are Biomarkers of Oxidative Stress and Linked to Impaired Membrane Integrity in Avian Red Blood Cells.

Oxidative stress is generally understood to be an important mediator of life-history traits, yet the specific relationships between oxidative stress and life-history traits have been difficult to describe because there is often a lack of covariation among biomarkers of oxidative stress. For instance, although oxidative damage to red blood cell (RBC) membranes can lead to pathological conditions (i.e., anemia), in some cases there is not a clear relationship between lipid oxidation and RBC membrane resistance to pro-oxidants. Alternatively, oxidative damage to hemoglobin may be an indirect mechanism contributing to RBC membrane damage. To better understand the mechanisms contributing to oxidative damage and probe new approaches to measuring oxidative stress, we used a series of in vitro and in vivo procedures in zebra finches (Taeniopygia guttata) to explore (1) whether avian RBCs exposed to a pro-oxidant generate fluorescent heme degradation products (HDPs), (2) whether HDPs interact with RBC membranes, and (3) whether HDPs are linked to impaired RBC integrity. We found that finch RBCs exposed in vitro to hydrogen peroxide produced fluorescent HDPs and HDPs associated with RBC membranes. Exposure to hydrogen peroxide also caused a reduction in hemoglobin and an increase in percent methemoglobin (a hemoglobin oxidation product), further indicating hemoglobin degradation. Moreover, HDP fluorescence correlated with impaired membrane integrity and erythrocyte osmotic fragility in vivo. This study suggests that reactive oxygen species may indirectly impair RBC membrane integrity via hemoglobin degradation products that associate with RBC membranes and that HDPs may be an inexpensive and logistically simple tool for measuring oxidative stress.

Methaemoglobinemia Induced by Poppers and Bupropion Intoxication in the Emergency Department.

A 40-year-old man presented to the emergency department with dyspnoea and fatigue after bupropion and popper consumption. Clinical examination was remarkable for central cyanosis not responding to supplementary oxygen. Arterial blood gas analysis showed a methaemoglobin value of 30.3%. Methaemoglobinemia was diagnosed and the patient was treated with methylene blue. However, during methylene blue administration, the patient developed a generalized tonic-clonic seizure that was successfully managed with diazepam. Combined intoxications can be a critical problem in the emergency department. Early recognition and treatment of poisoning are key for good patient outcome.LEARNING POINTSDistinguishing toxidromes is critical for adequate treatment of patients with drug intoxication; the most common side effect of bupropion consumption is dose-dependent seizures.The diagnosis of methaemoglobinemia requires a high index of suspicion, particularly in a patient presenting with central cyanosis not responding to supplementary oxygen.Treatment with methylene blue is recommended when the percentage of methaemoglobin is above 30% or when the patient has symptoms related to methaemoglobinemia.

Subacute intoxication with sodium nitrate induces hematological and biochemical alterations and liver injury in male Wistar rats

Nitrate pollution has emerged as a problem of great importance because in recent years, the levels of nitrate in soil and groundwater have increased, mainly through anthropogenic activities, such as the use of fertilizers in agriculture, domestic wastewater and septic tanks, industrial waste and deforestation. In animals, nitrate reduction to nitrite (NO2) and nitric oxide (NO) promote the formation of methemoglobin in the blood and the generation of highly reactive intermediates that induce oxidative stress in target organs. Exposition to nitrates has been associated with methemoglobinemia, reproductive toxicity, metabolic and endocrine alterations and cancer. This study analyzed acute intoxication with sodium nitrate (NaNO3) in male Wistar rats, aged 12–16 weeks. Four groups with n = 10 rats each were formed: group 1 was the control, and group 2, group 3 and group 4 were treated for 10 days with intragastric doses of 19, 66 and 150 mg/kg/d NaNO3, respectively. Hematological, metabolic and histological biomarkers in the liver were analyzed. The results showed high percentages of methemoglobin, an increase in NO2 in the plasma and an accumulation in the liver. Moreover, there were high counts of white blood cells and platelets in all treated groups. Additionally, there was an increase in the spleen weight in group 4. High levels of glucose, triglycerides, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed and were significantly increased in groups 3 and 4. For oxidative stress biomarkers, there were increases in Thiobarbituric Acid Reactive Substances (TBARS), total GSH and SOD activity, mainly in group 4. Changes in mitochondrial activity were not significant. Histopathological analyses of the liver showed inflammation, infiltration of mononuclear cells, steatosis, ischemia and necrosis, and these findings were more evident at high doses of NaNO3 in which high of S-nitrosylation were found. In conclusion, NaNO3 was reduced to NO2, thereby inducing methemoglobinemia, whereas other reactive species generated oxidative stress, causing hematological and metabolic alterations and injury to the liver.

Failure of Pulse Oximetry and Cooximetry as Monitors in a Patient With Hemoglobin MIwate: A Case Report.

We present the perioperative details of a 2-year-old child scheduled for cleft palate repair. Low pulse oximetry readings after induction of anesthesia and before surgery led to the diagnosis of HbMIwate, a rare congenital methemoglobinemia due to mutation in the α-globin gene. We explored the utility of noninvasive cooximetry to monitor methemoglobin and oxygenation during anesthesia and found that noninvasive cooximetry is not useful to monitor oxygenation or to detect the percentage of methemoglobin arising from congenital variants like HbMIwate.

Nitrate poisoning in ruminants

This paper describes the nitrate - nitrite poisoning of ruminants. This disease is caused by the ingestion of large amount of nitrate salts, which are reduced in the rumen to nitrite ions. Nitrites, after their absorption, cause the formation of methemoglobin and, in turn, respiratory and circulatory distress. The aim of the treatment is to reduce the percentage of methemoglobin in blood and to stop the continuing production of nitrite ions in the rumen. For the prevention of the disease, avoidance of feedstuff rich in nitrates and improvement of the water quality, are suggested.

Enzymopenic Congenital Methemoglobinemia in Children of the Republic of Sakha (Yakutia)

Type I congenital methemoglobinemia is an autosomal recessive disorder. A high frequency of congenital methemoglobinemia has been reported among Native Americans inhabiting the Yukon-Kuskokwim Delta. Other rare cases of congenital methemoglobinemia of types I and II have been reported in Japan and other countries. In Russia-namely, in Yakutia-a high frequency of type I congenital methemoglobinemia has been reported. In 2009, the Consultation Polyclinic of the Pediatric Center in Yakutsk city established a registry of children with congenital methemoglobinemia. In total, 43 patients were registered between 2005 and 2009. The median methemoglobin level was 13.5% (ranging between 4.2% and 33.9%) and physical examination revealed cyanosis of the skin and mucus membranes. There were significant positive relationships between percentage of methemoglobin and erythrocyte count, hemoglobin concentration, and hematocrit among male patients, consistent with an upregulation of the hypoxic response. The prevalence per 100,000 children ranged from 12.7 to 47.0 in 3 geographic regions of Yakutia. Further research is needed to clarify the clinical consequences of congenital methemoglobinemia in the children of Yakutia and the reasons for the high variability in the prevalence of the condition.

Detecting Methemoglobinemia in Animals with a Drop of Blood.

A major concern during pesticide development and use is the impact on non-target species, such as raptors or domestic cats and dogs. Sodium nitrite and para-aminopropiophenone (PAPP) are two toxicants currently being studied for the control of invasive species, such as starlings and feral swine. When given to an animal these compounds oxidize hemoglobin, which renders it unable to carry oxygen resulting in methemoglobinemia. This study developed a method to estimate methemoglobin levels in mammals and birds by examining the efficacy of sodium nitrite to induce the conversion of hemoglobin to methemoglobin. Varying concentrations of sodium nitrite were added to aliquots of coyote, vole, feral swine, starling, and duck blood, collected from captive animals. The blood samples were analyzed spectrophotometrically to determine percent methemoglobin and digitally to determine red color values (RCV) associated with different methemoglobin levels. The avian and mammalian blood reached 100% methemoglobin levels at 200 mM and 15 mM sodium nitrite, respectively. All animals had similar RCV for a given percent methemoglobin. In conclusion, this study developed a procedure to quickly determine methemoglobin levels in mammals and birds. Furthermore, percent methemoglobin can be estimated with one standard curve from any animal species and an image of a blood spot. The technique will be useful during field studies, in agricultural areas, or in a veterinarian’s office for the rapid diagnosis of methemoglobinemia in non-target animals that have eaten toxicants/baits or baited animals.

Role of DPP (Phoenix dactylifera L.) extract on Ameliorating The incidence of hemoglobinoxidation induced by sodium nitrite

The effects of ethanolic extract of date palm pollen grains(DPP) was investigated on the ameliorating the oxidative effect of sodium nitrite on hemoglobin in albino mature female rats , twenty four(24) rats weighing 150- 200 g were grouped into four groups two control and two experimental groups, first group(GI) considered as negative control received 0.5 ml distilled water and after 45 minutes received another 0.5 ml of distilled water while the second control group(GII), (positive control) received 0.5 ml of distilled water then after 45 minutes received 100mg/kg Body weight sodium nitrite. While the two experimental groups were treated as follow, first treated group(GIII) received 100mg/kg Body weight crude ethanolic extract of DPP then after 45 minutes received 100mg/kg Body weight sodium nitrite. while second(GIV) treated group received 100mg/kg Body weight crude ethanolic extract of DPP daily for seven days then after 45 minutes from last dose received 100mg/kg B.W. sodium nitrite. Whole blood samples were obtained in heparinized tubes to detect methemoglobin percentage. The results in animals treated with single oral dose (100mg/Kg) of sodium nitrite comprised 45% met-Hb, 45 minutes after nitrite treatment, while animal,s group pretreated with ethanolic extract of DPP in a dose of 100mg/kg for seven consecutive days given as single oral dose of sodium nitrite after 45 minutes from last dose (before induction of methemoglobinemia) by nitrite administration revealed an increases in the level of met-Hb percentage in blood compared to that of control group treated with distilled water before sodium nitrite. However the percent inhibition of met-Hb formation over long term treatment was less than that observed with short term treatment.

Noninvasive photoacoustic microscopy of methemoglobin in vivo.

Due to the various causes of methemoglobinemia and its potential to be confused with other diseases, in vivo measurements of methemoglobin have significant applications in the clinic. Using photoacoustic microscopy (PAM), we quantified the average and the distributed percentage of methemoglobin both in vitro and in vivo. Based on the absorption spectra of methemoglobin, oxyhemoglobin, and deoxyhemoglobin, three wavelengths were chosen to differentiate methemoglobin from the others. The methemoglobin concentrations calculated from the photoacoustic signals agreed well with the preset concentrations. Then we imaged the methemoglobin percentage in microtubes that mimicked blood vessels. Average percentages calculated for five samples with different methemoglobin concentrations also agreed well with the preset values. Finally, we demonstrated the ability of PAM to detect methemoglobin in vivo in a mouse ear. Our results show that PAM can quantitatively image methemoglobin distribution in vivo.

Exposição ocupacional ao difluobenzuron: avaliação de metemoglobina após a jornada de trabalho dos guardas de endemias atuantes na região do grande Rio de Janeiro

Atualmente, a substância utilizada para o combate do vetor da dengue é o diflubenzuron, um larvicida que possui como principal efeito no ser humano a formação demetemoglobina. A determinação do percentual de metemoglobina (MHb) no sangue permite estabelecer a relação com a exposição ao diflubenzuron, sendo utilizada como indicador de efeito. O objetivo do presente trabalho foi avaliar a efetividade do uso da MHb como indicador da exposição ao diflubenzuron por meio da determinação de sua concentração no sangue de guardas de endemias atuantes em dois municípios do Estado do Rio de Janeiro. Para a avaliação da MHb, foi utilizado o método de análise preconizado por Evelyn-Malloy, a espectrofotometria no visível λmáx=630 nm, e as informações complementares foram obtidas por intermédio da aplicação de questionários semiestruturados. Foi observado que a maioria dos trabalhadores não fazia uso de Equipamento de Proteção Individual (EPI) e atuava em condições de trabalho insalubres e sem treinamento adequado. Houve redução de cerca de 0,05% da concentração da MHb após a exposição ao diflubenzuron, com correlação inversa deste indicador de efeito com a variável fumo (R= -0,742; p=0,035). Dado que a MHb pode ser formada após exposição a diversas substâncias químicas e considerando as dificuldades na logística de execução desta análise, estudos sobre novos biomarcadores mais sensíveis e seletivos são necessários.

English

Humans are exposed to a number of toxic elements in the environment. Cadmium, widely used in industry, is a great environmental health problem of both humans and animals. Effects of reactive oxygen species (ROS) generation have been postulated to be major contributors to cadmium-exposure related disease. The aim of this study was to investigate the effect of curcumin on oxidative stress in rats exposed to cadmium. Curcumin was administered orally (600 mg/kg body weight). After 24 days, significant increases in methemoglobin percentage (metHb%), superoxide dismutase (SOD), glutathione peroxidase (GPx) activity, malondialdehyde (MDA) concentration and hemolysis test were observed in cadmium exposed rats compared to control group (P < 0.05), while GSH concentration showed insignificant change. Curcumin treatment of cadmium exposed rats significantly lowered metHb%, while significantly increased oxyhemoglobin percentage (HbO2%), compared to cadmium alone group (P < 0.05). Also curcumin treatment significantly increased GPx activity of cadmium exposed rats as compared to cadmium alone group (P < 0.05). Curcumin treatment of cadmium exposed rats lowered MDA concentration and hemolysis percentage by 10 and 9%, respectively. The findings of this study suggest that curcumin elevated the GPx activity of cadmium exposed rats and had ameliorative effect on lipid peroxidation and erythrocytes hemolysis. Moreover, the results of multi-component spectrophotometric analysis suggest that curcumin treatment of lead exposed rats lowered the levels of inactive metHb level and elevated the level of active HbO2. Curcumin may exert its protective actions against cadmium-induced hematotoxicity in rats possibly through its antioxidant mechanisms and may have future therapeutic relevance. Key words: Cadmium, curcumin, oxidative stress, erythrocytes, hemolysis, Hb-derivatives, rats.

Haematological Alterations Induced by Oral Subacute Exposure to Fenvalerate, Nitrate and Their Combination in Domestic Buffalo, Bubalus bubalis

The present study investigated haematological alterations induced by oral subacute exposure to fenvalerate, nitrate and their combination in the domestic buffalo, Bubalus bubalis. Fenvalerate exposure produced significant declines in haemoglobin (Hb), total leukocyte count (TLC), total erythrocyte count (TEC) and mean corpuscular haemoglobin concentration (MCHC), and a corresponding elevation in mean corpuscular volume (MCV). Following oral exposure to sodium nitrate, significant declines in blood Hb, TLC, TEC, MCH and MCHC, and a significant elevation in MCV occurred. Combined exposure to fenvalerate and sodium nitrate produced severe effects with an appreciably more prominent decline in Hb, TLC, TEC and MCHC and a significant elevation in MCV. The percentage of methaemoglobin was observed to follow an elevating trend in animals exposed to sodium nitrate alone (0.69 %-13.8 %) and in combination with fenvalerate (0.75 %-13.7 %).

Antioxidant effect of zinc supplementation on both plasma and cellular red-ox status markers in a group of elderly Italian population.

The aim of this work was to evaluate the effect of long term supplementation with two moderate dose of Zn on plasma and cellular red-ox status markers in elderly volunteers. In a double blind study 108 healthy volunteers, aged 70-85 years, were enrolled. They were randomly divided in 3 groups of treatment, receiving placebo, 15 mg/day and 30 mg/day of Zn for 6 months. Red-ox status markers were assessed at baseline and after 6 months evaluating carotenoids, vitamin A and E in plasma; glutathione (GSH), thiol groups (RSH), malondialdehyde (MDA), percentage of haemolysis and methemoglobin in erythrocytes. Zn supplementation had no significant effects on red-ox status markers except for vitamin A levels (from 1.94±0.44 to 2.18±0.48 μM in volunteers receiving 15 mg of Zn and from 1.95±0.46 to 2.26±0.56 μM in volunteers receiving 30 mg of Zn), which increased proportionally to zinc dose. It appears that, differently from unhealthy populations, long-term supplementation with two moderate doses of Zn in a healthy elderly population, with an adequate Zn nutritive status and macro and micronutrients intakes in the range of normality, is an inefficient way to increase antioxidant defences.

A dietary flavanone glycoside naringin modulates the abnormalities of human erythrocytes exposed with deltamethrin, by upregulating the expression of antioxidants

The protective effect of naringin on deltamethrin poisoning in human erythrocyte was studied using an in vitro model. Hemolysis, percentage met-hemoglobin, lipid peroxidation, glutathione, antioxidant enzymes and erythrocyte ghost protein pattern were assessed to investigate the effect of naringin. Erythrocytes at a hematocrit of 10% were incubated with 500ppm of deltamethrin and/or 0.1M naringin under physiological conditions of temperature and pH for 2h. Deltamethrin significantly increased the percentage of hemolysis and met-hemoglobin in human erythrocytes as compared to the control erythrocytes and naringin significantly (P<0.05) inhibited the percentage of hemolysis and met-hemoglobin. The levels of lipid peroxides and conjugated diene increased whereas the level of glutathione decreased significantly (P<0.05) by deltamethrin-incubated erythrocytes. Naringin significantly inhibited the formation of lipid peroxides and conjugated diene while increased the glutathione level in erythrocytes incubated with deltamethrin. The activity of antioxidant enzymes and non-enzymic antioxidants were decreased in erythrocytes incubated with deltamethrin whereas naringin improved the activities of these antioxidant and non-enzymic antioxidants. SDS–PAGE of erythrocyte ghost protein pattern showed an alteration in the protein bands by deltamethrin poisoning but naringin significantly inhibited the alteration in protein profile. The present study divulges that naringin can reduce the abnormalities of deltamethrin poisoning by ameliorating oxidative stress. This finding raises the possibility that naringin may provide protection from pesticide poisoning.