RESUMO
The aim of this study was to understand the effects of zinc supplementation on antioxidant defense systems, hematological indices, and erythrocyte morphology in conditions of chronic arsenic toxicity. Male Wistar rats were segregated into four groups: control, arsenic treated, zinc supplemented, and arsenic + zinc treated. The animals in the arsenic-treated group were given arsenic orally in drinking water in the form of sodium arsenite at a dose level of 100 mg L-1, and zinc was administered to zinc-treated animals in the form of zinc sulfate orally in drinking water at a dose level of 227 mg L-1. The animals were subjected to different treatments for a period of 12 weeks, and various investigations were undertaken that included serum zinc content, activity of antioxidant enzymes, and hematological indices. Further, scanning electron microscopic (SEM) studies were performed to assess morphological changes in erythrocytes. Arsenic treatment significantly reduced serum zinc concentrations, which, however, were restored to near-normal levels upon zinc supplementation. The activities of enzymes involved in antioxidant defense systems were altered in the erythrocyte lysates of arsenic-treated rats, which interestingly revealed a significant improvement upon simultaneous zinc supplementation. A significant reduction in the counts of total leukocytes, neutrophils, and lymphocytes was observed following arsenic intoxication, which came back to near control levels following zinc supplementation. Also, protective effects of zinc were evident from SEM that revealed maintenance of topographical appearances of erythrocytes in conditions of arsenic toxicity. Thus, this study clearly shows the protection afforded by zinc on erythrocytes during arsenic-induced toxicity.
Assuntos
Arsênio/toxicidade , Eritrócitos/efeitos dos fármacos , Zinco/farmacologia , Animais , Catalase/metabolismo , Eritrócitos/patologia , Eritrócitos/ultraestrutura , Glutationa/sangue , Glutationa Transferase/metabolismo , Hemoglobinas/análise , Contagem de Leucócitos , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Microscopia Eletrônica de Varredura , Ratos , Ratos WistarRESUMO
OBJECTIVE: In this study, we have investigated the role of zinc supplementation (a nutritional antioxidant) in an ovariectomized osteopenic rat model. METHODS: Forty-eight female Wistar rats were assigned to four groups: control, zinc, ovariectomy (OVX), and OVX + zinc. Analysis was performed to compare the study groups on bone metabolism markers, bone antioxidant enzymes, and zinc and copper levels in serum and bone tissues. Electron microscopy was also performed to assess morphological changes. RESULTS: Estradiol levels decreased and tartarate-resistant acid phosphatase 5b levels increased in the OVX group. In the OVX + zinc group, these levels were regulated; however, estradiol levels were still significantly lower than those in controls. The OVX group showed significantly higher urinary excretion of hydroxyproline, which recovered upon zinc supplementation but was higher than normal levels. The activities of catalase and superoxide dismutase decreased in ovariectomized animals and up-regulated upon zinc supplementation. Zinc supplementation in the OVX group revoked reduced glutathione levels and elevated malondialdehyde levels. Reduction in zinc and copper levels was observed in the bone tissues and serum of the OVX group. Zinc administration restored these levels to normal. Electron microscopic studies revealed a looser structure and resorbed areas in ovariectomized rat cortical bone. Zinc administration restored bone tissue morphology. CONCLUSIONS: These findings suggest that changes in cortical bone attributed to estrogen deficiency are arrested by zinc supplementation, which can be a sustainable approach to improving bone health.
Assuntos
Modelos Animais de Doenças , Osteoporose Pós-Menopausa/tratamento farmacológico , Osteoporose Pós-Menopausa/prevenção & controle , Oligoelementos/administração & dosagem , Zinco/administração & dosagem , Animais , Catalase/efeitos dos fármacos , Feminino , Glutationa/efeitos dos fármacos , Humanos , Hidroxiprolina/urina , Ovariectomia , Distribuição Aleatória , Ratos , Ratos Wistar , Superóxido Dismutase/efeitos dos fármacosRESUMO
AIM: To determine oxidant stress and antioxidant capacity in chronic pancreatitis (CP) patients with and without diabetes mellitus. METHODS: This study is a secondary data analysis of our earlier study on 127 (male = 86) patients with CP, grouped as those with diabetes (case; n = 23) and those without diabetes (control). Markers of antioxidant status included vitamins A and E, total antioxidant capacity (TAC; measured as ferric-reducing ability of plasma [FRAP]), and total glutathione (T-GSH). Markers for oxidative stress included lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS) and serum superoxide dismutase (s-SOD). RESULTS: Patients with diabetes were older (mean [SD] age 36.4 [9.7] vs. 29.3 [10.0] years; p = 0.032), had longer duration of CP [4 (0.3-21) vs. 3 (0.3-24) years; p = 0.07), and had a lower TAC (269.8 [92.4] vs. 355.5 [128.6] µmoles Fe(+2) liberated; p = 0.003) compared to those without diabetes. In multiple logistic regression analysis taking all exploratory variables, FRAP (<270 µmoles Fe(+2) liberated) was associated with diabetes independent of duration of CP, age of patients, and TBARS levels. However, oxidative stress levels were not different between diabetic and nondiabetic patients. CONCLUSIONS: Diabetes was found to be associated with longer duration of CP and with low antioxidant capacity. Further studies will be needed to evaluate a causal association.
Assuntos
Antioxidantes/metabolismo , Diabetes Mellitus/diagnóstico , Glutationa/sangue , Estresse Oxidativo/fisiologia , Pancreatite Crônica/diagnóstico , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Adulto , Biomarcadores/sangue , Estudos de Casos e Controles , Intervalos de Confiança , Diabetes Mellitus/epidemiologia , Progressão da Doença , Feminino , Seguimentos , Humanos , Peroxidação de Lipídeos/fisiologia , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Razão de Chances , Pancreatite Crônica/epidemiologia , Valores de Referência , Medição de Risco , Índice de Gravidade de Doença , Adulto JovemRESUMO
BACKGROUND: Oxidative stress (OS) in acute pancreatitis (AP) has been pathologically linked with the systemic inflammatory response and antioxidant supplementation may have a clinical benefit. METHODS: In this prospective, randomised open label, controlled pilot study, patients admitted within 72 hours of onset of pain were randomised to receive either placebo (only standard medical treatment; SMT) or antioxidants (vitamin C 500 mg, N-acetyl cysteine 200 mg 8 hourly and antoxyl forte 1 capsule hourly with standard medical treatment; SMT + AO) daily, following informed consent. Patients with co-morbid illness and pregnancy were excluded. Primary efficacy measures were length of hospital stay and complications whilst secondary measures were biochemical markers of oxidative stress (thiobarbituric acid reactive substances [TBARS] and superoxide dismutase [SOD] and total antioxidant capacity [TAC] and vitamin C) at Days 1, 3 and 7. RESULTS: Of 53 patients, 30 patients were randomised to SMT and 23 patients to SMT + AO. The mean duration of hospital stay in the SMT group (10.3 +/- 7 days) was more compared to SMT + AOT (7.2 +/- 5 days), but was not statistically significant (p=0.07), complications were similar in the 2 groups. At Day 7, OS was significantly lower in the SMT + AO group when compared with the SMT group (TBARS, p=0.05; SOD, p=0.03) with a significant increase in FRAP and vitamin C (p=0.01). CONCLUSIONS: Antioxidant supplementation may decrease the length of hospital stay and complication rate in patients with AP, but a larger clinical trial is needed to support this hypothesis. Further, it decreased the OS and improved the antioxidant status in patients with AP.
Assuntos
Acetilcisteína/uso terapêutico , Antioxidantes/uso terapêutico , Ácido Ascórbico/uso terapêutico , Pancreatite/tratamento farmacológico , Doença Aguda , Adulto , Biomarcadores/sangue , Feminino , Humanos , Tempo de Internação/estatística & dados numéricos , Masculino , Estresse Oxidativo , Pancreatite/complicações , Projetos Piloto , Placebos , Estudos Prospectivos , Estatísticas não Paramétricas , Resultado do TratamentoRESUMO
Increased oxidative stress has been postulated to be an important mechanism in the pathophysiology of chronic pancreatitis (CP). Micronutrient deficiency may increase the oxidative stress as they assist in free radical clearance. The present study was undertaken to assess the intake of micronutrients, i.e. vitamins E and C, carotene, selenium, copper, zinc, manganese, magnesium, sulphur, riboflavin, methionine and choline in patients with CP. All consecutive patients with CP attending the Pancreas Clinic at the All India Institute of Medical Sciences were enrolled in the study. The usual dietary intake was estimated by the 24-hour dietary recall method and food frequency questionnaire. Dietary restrictions, if any, were also noted. The micronutrient intake of patients not on any nutritional supplements (n=75, 65 males and 10 females, mean age 31.06 +/- 10.64 years) was compared with age- and sex- matched healthy controls (n=75). The micronutrients were calculated as per the Nutritive value of Indian Foods given by the National Institute of Nutrition, Indian Council of Medical Research, India and the US dietary intake guidelines as applicable. It was found that the Body Mass Index (BMI) of patients was significantly lower than that of healthy controls. The total intake in terms of calorie was lower in patients when compared to controls. The dietary intake of vitamin E, riboflavin, choline, magnesium, copper manganese and sulfur was significantly lower than that of controls as well as the Recommended Dietary Allowance (RDA). Dietary intake of selenium and vitamin C was within the limits of the RDA but was lower than that of controls, while the intake of carotene was similar in both the groups and met the RDA. We conclude that patients with CP had significantly decreased micronutrient intake owing to diet modification due to pain. Micronutrient deficiency might contribute to increased oxidative stress in these patients.