Background: Chronic exposure to silica is related with the provocation of an inflammatory response and oxidative stress mechanism. Vitamin D has multiple benefits in biological activities particularly respiratory system disease. Method: In this research, 20 male Wistar rats were randomly allocated into four groups (5 rats /group) as follow: Group1 received saline as (negative control) group. The group 2 received a single IT instillation of silica (positive control) group; the group 3 was co-administrated with single IT silica and Vitamin D (20 mg/kg/day) daily for a period of 90 days. The rats of group 4 received Vitamin D daily for a period of 90 days. Results: Silica significantly increased serum and lung total Oxidant Status (TOS). Meanwhile, silica reduced serum and lung total antioxidant capacity (TAC), GSH and tumor necrosis factor-α (TNF-a). Vitamin D treatment meaningfully reversed oxidative stress, antioxidants status and inflammatory response. Also, Vitamin D improved histopathological changes caused by silica. Conclusion: These findings indicate that Vitamin D exerts protective effects against silica-induced lung injury. It seems that Vitamin D has potential use as a therapeutic object for silica induced lung injure.
Impaired fasting glucose (IFG) is one of significant risk factors of developing diabetes. The persons with IFG are, thus, an important target group for primary prevention of diabetes. It is well known that plasma homocysteine concentration may be increased in poor folate nutritional status. Elevated level of plasma homocysteine is considered as a marker of enhanced oxidative stress. In addition, the protective effect against oxidative stress may be diminished in poor antioxidative nutrient status as vitamin C. It is, therefore, important to maintain adequate nutritional status of folate and vitamin C in the patients with type 2 diabetes or IFG. This study was performed to determine the effects of supplementation of folic acid or vitamin C on plasma concentrations of homocysteine, oxidized LDL, and lipids and on the activity of plasma anti-oxidative enzyme in patients with IFG. A total of 97 patients with IFG were participated voluntarily with written consents. They were divided into one of the four experimental groups; Control (C), Folatesupplemented (F), Ascorbate-supplemented (A), and Folate plus ascorbate-supplemented (FA). The subjects in C were taken placebo, those in F were supplemented 1 mg of folate, those in A were received 1,000 mg of vitamin C, and those in FA were given 1 mg of folate plus 1,000 mg of vitamin C daily for 4 weeks. No change in plasma concentrations of vitamin C, lipids, and oxidized LDL and the activity of GSH-Px were observed in vitamin C-supplemented group (A + FA) and folate-supplemented group (F + FA) compared to the placebo group (C + A). Only the folate-supplemented group (F + FA) had significantly increased average serum folate concentration and lowered plasma homocysteine concentration compared to the placebo group (C + A). Thus, it should be recommended the patients with IFG to increase folate intake through diets and, if it is not sufficient, to take folic acid supplements to prevent the development of complications induced by hyperhomocysteinemia as well as oxidative stress.
Glutathione S-transferase (GST) is a multigene family of phase II detoxifying enzymes that metabolize a wide range of exogenous and endogenous electrophilic compounds. GSTM1 and GSTT1 gene polymorphisms may account for inter-individual variability in coping with oxidative stress. We investigated the relationships between the level of lymphocyte DNA and antioxidative parameters and the effect on GST genotypes. GSTM1 and GSTT1 were characterized in 301 young healthy Korean adults and compared with oxidative stress parameters such as the level of lymphocyte DNA, plasma antioxidant vitamins, and erythrocyte antioxidant enzymes in smokers and non smokers. GST genotype, degree of DNA damage in lymphocytes, erythrocyte activities of superoxide dismutase, catalase, and glutathione peroxidase (GSH-Px), and plasma concentrations of total radical-trapping antioxidant potential (TRAP), vitamin C, ${\alpha}$- and ${\gamma}$-tocopherol, ${\alpha}$- and ${\beta}$-carotene, and cryptoxanthin were analyzed. Lymphocyte DNA damage assessed by the comet assay was higher in smokers than that in non-smokers, but the levels of plasma vitamin C, ${\beta}$-carotene, TRAP, erythrocyte catalase, and GSH-Px were lower than those of non-smokers (p < 0.05). Lymphocyte DNA damage was higher in subjects with the GSTM1- or GSTT1-present genotype than those with the GSTM1-present or GSTT1- genotype. No difference in erythrocyte antioxidant enzyme activities, plasma TRAP, or vitamin levels was observed in subjects with the GSTM1 or GSTT1 genotypes, except ${\beta}$-carotene. Significant negative correlations were observed between lymphocyte DNA damage and plasma levels of TRAP and erythrocyte activities of catalase and GSH-Px after adjusting for smoking pack-years. Negative correlations were observed between plasma vitamin C and lymphocyte DNA damage only in individuals with the GSTM1-present or GSTT1- genotype. The interesting finding was the significant positive correlations between lymphocyte DNA damage and plasma levels of ${\alpha}$-carotene, ${\beta}$-carotene, and cryptoxanthin. In conclusion, the GSTM1- and GSTT1-present genotypes as well as smoking aggravated antioxidant status through lymphocyte DNA damage. This finding confirms that GST polymorphisms could be important determinants of antioxidant status in young smoking and non-smoking adults. Consequently, the protective effect of supplemental antioxidants on DNA damage in individuals carrying the GSTM1- or GSTT1-present genotypes might show significantly higher values than expected.
Ki, Young-Sun;Min, Jin-Young;Yoo, Hong-Sik;Paek, Do-Myung
Journal of Environmental Health Sciences
/
v.34
no.2
/
pp.117-123
/
2008
Allergic diseases have been dramarically increased over recent years, especially in industrialized countries. Oxidative stress has been believed to playa significant role in the occurrence of the allergic inflammatory responses. Although previous studies concerning oxidative stress and systemic inflammation have been reported, few data is available, and other allergic diseases, except for asthma, are hardly studied about the association with oxidative stress. This study evaluated the relationship between allergic disease and Malondialdehyde (MDA) as an indicator of oxidative stress. The study population was 197 male adults living in an industrial area. The ISAAC questionnaire was used to confirm wheezing and rhinitis, and atopy was evaluated by skin prick test. MDA was analyzed by spectrophotometer. To examine bronchial hyperresponsiveness (BHR), methacholine test was performed, and the index of bronchial responsiveness (BR index) was calculated. We used multivariate logistic regression model and general linear model with SAS program. We found significant associations of MDA with brindex (p=0.023), rhinitis (p=0.016), atopy (p=0.03), adjusted by age, smoking, and body mass index (BMI). On the contrary, there was no significant difference of MDA with the status of asthma. Our result suggests that oxidative stress may playa major role in the occurrence of allergic response in male adults.
Garcia, Elisa Mariana;Lopez, Agustin;Zimerman, Maria;Hernandez, Olegario;Arroquy, Jose Ignacio;Nazareno, Monica Azucena
Asian-Australasian Journal of Animal Sciences
/
v.32
no.9
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pp.1439-1447
/
2019
Objective: The aim of this study was to evaluate the effect of dietary incorporation of tanninrich woody species on meat oxidative stability, carcass traits and meat quality in goats. Methods: Two tannin-rich species were tested using a three-treatments feeding trial, where treatments consisted of: Larrea divaricata and Acacia aroma both at 12.5% in dry matter basis of the diet and a control diet (alfalfa hay). All feeding diets were iso-protein and iso-energy. Carcass conformation, carcass compactness, carcass fatness and subcutaneous fat deposition were evaluated. Intake, liveweigh, Longissimus thoracis et lumborum muscles of goats were analyzed in order to evaluate quality parameters such as pH value, instrumental color evaluation, water holding capacity, total phenolic content, antioxidant activity, meat oxidative stability and fatty acid profiles in meat. Results: Feed intake, liveweight gain, carcass, and meat traits did not differ among treatments. Changes in meat lipid profile among treatments were observed for oleic and elaidic acid contents. Meat total phenolic content and antioxidant activity did not differ among treatments; although, meat oxidative status after storage at room temperature, as well as under refrigerated and frozen conditions were different between control and both supplemented groups. Conclusion: The inclusion of Acacia aroma and Larrea divaricata leaves in goat diet enhanced meat oxidative stability. Modulation of the ruminal biohydrogenation of fatty acids produced by condensed tannins of these plant species need to be further investigated.
The present study was designed to observe the effect of chronically ingested ethanol on the level of fatty acid ethyl esters (FAEEs), which is a non-oxidative metabolite of ethanol metabolism in tissues, and its correlation to the status of oxidative stress in rats. Forty male Sprague Dawley rats weighing 145 - 155 g were divided into 2 groups, Control and EtOH. All rats were fed Lieber-DeCarli liquid diet for 4 weeks by pair-feeding. An isocaloric maltose dextrin was added in replace of 50 g ethanol (36%kcal) in the control diet. Chronically ingested ethanol significantly increased the content of FAEEs in pancreas and liver, but not in brain. The level of 2-thiobarbituric acid reactive substances (TBARS) was significantly increased, but ${\alpha}-tocopherol$ level was significantly decreased in pancreas and liver. However, the levels of TBARS and ${\alpha}-tocopherol$ in brain were not significantly affected by ethanol ingestion. Therefore, chronically ingested ethanol might cause tissue damage by increasing the levels of FAEEs and TBARS and dissipating more ${\alpha}-tocopherol$ in tissues.
Mitochondrial dysfunction is closely associated with reactive oxygen species (ROS) generation and oxidative stress in cells. On the other hand, modulation of the cellular antioxidant defense system by changes in the mitochondrial DNA (mtDNA) content is largely unknown. To determine the relationship between the cellular mtDNA content and defense system against oxidative stress, this study examined a set of myoblasts containing a depleted or reverted mtDNA content. A change in the cellular mtDNA content modulated the expression of antioxidant enzymes in myoblasts. In particular, the expression and activity of glutathione peroxidase (GPx) and catalase were inversely correlated with the mtDNA content in myoblasts. The depletion of mtDNA decreased both the reduced glutathione (GSH) and oxidized glutathione (GSSG) slightly, whereas the cellular redox status, as assessed by the GSH/GSSG ratio, was similar to that of the control. Interestingly, the steady-state level of the intracellular ROS, which depends on the reciprocal actions between ROS generation and detoxification, was reduced significantly and the lethality induced by $H_2O_2$ was alleviated by mtDNA depletion in myoblasts. Therefore, these results suggest that the ROS homeostasis and antioxidant enzymes are modulated by the cellular mtDNA content and that the increased expression and activity of GPx and catalase through the depletion of mtDNA are closely associated with an alleviation of the oxidative stress in myoblasts.
Early onset of Batten disease (EBD), one of the most lethal neurodegenerative storage disorders of childhood, is caused by inactivating mutations in the Ceroid Lipofuscinosis, Neuronal (CLN1) gene. Neurogranin, a calmodulin-binding protein, is expressed in the brain and participates in the protein kinase C (PKC) signaling pathway. While oxidative stress is the suggested cause of neurodegeneration in EBD, its molecular mechanism(s) remains obscure. In this research, we examined the levels of neurogranin in the brain mRNA of wild-type (WT) mice and EBD knockout (KO) mice, as well as the proteins. We also performed neuronal cultures to measure the expression levels of neurgranin and phosphorylated-neurogranin with or without oxidative stress inducers and anti-oxidants. Results showed that neurogranin in both EBD KO mice brain mRNA and protein extracts decreased in an age dependent manner. However, high amounts of phosphorylated-neurogranin were detected in the 6-month brain. This pattern was also confirmed by cultured neurospheres samples. Moreover, neurospheres treated with $H_2O_2$, an oxidative stress inducer, showed increased phosphorylated-neurogranin patterns. Interestingly, this pattern returned to normal status when treated with N-acetyl-L-cystein, an anti-oxidant, after $H_2O_2$ treatment was performed. Our results suggest that the phosphorylation of neurogranin is affected by oxidative stress status in EBD, and appropriate anti-oxidant treatment will relieve hyper-phosphorylation of neurogranin.
Non-alcoholic fatty liver disease (NAFLD) is caused by fat accumulation and is associated with oxidative stress. In this study, we investigated the potential protective effect of pomegranate (Punica granatum L.) peel extract (PPE) against oxidative stress in the liver of rats with NAFLD. Sprague-Dawley rats were fed a high fat diet (HFD), 20% corn oil, or palm oil for 8 weeks in the presence or absence of PPE. The control group was fed a basal diet. The progression of NAFLD was evaluated histologically and by measuring liver enzymes (alanine transaminase and aspartate transaminase), serum lipids (triglycerides and total cholesterol), and oxidative stress markers. The HFD feeding increased the body weight and caused NAFLD, liver steatosis, hyperlipidemia, oxidative stress, and elevated liver enzymes. Administration of PPE ameliorated the hepatic morphology, reduced body weight, improved liver enzymes, and inhibited lipogenesis. Furthermore, PPE enhanced the cellular redox status in the liver tissue of rats with NAFLD. Our findings suggest that PPE could improve HFD-induced NAFLD via abolishment of hepatic oxidative damage and hyperlipidemia. PPE might be considered as a potential lead material in the treatment of NAFLD and obesity through the modulation of lipid metabolism.
Excessive oxidative stress and abnormal blood lipids may cause chronic diseases. This risk can be reduced by consuming an antioxidant- and fiber-rich vegetarian diet. We compared biomarkers of oxidative stress, antioxidant capacity, and lipid profiles of sex- and age-matched long-term vegetarians and omnivores in Korea. Forty-five vegetarians (23 men and 22 women; mean age, $49.5{\pm}5.3$ years), who had maintained a vegetarian diet for a minimum of 15 years, and 30 omnivores (15 men and 15 women; mean age, $48.9{\pm}3.6$ years) participated in this study. Their 1-day, 24-h recall, and 2-day dietary records were analyzed. Oxidative stress was measured by the levels of diacron reactive oxygen metabolites (d-ROM). Antioxidant status was determined by the biological antioxidant potential (BAP) and levels of endogenous antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. We observed that vegetarians had a significantly lower body fat percentage ($21.6{\pm}6.4%$) than that of omnivores ($25.4{\pm}4.6%$; $P$ < 0.004). d-ROM levels were significantly lower in vegetarians than those in omnivores ($331.82{\pm}77.96$ and $375.80{\pm}67.26$ Carratelli units; $P$ < 0.011). Additionally, total cholesterol levels in the vegetarians and omnivores were $173.73{\pm}31.42$ mg/dL and $193.17{\pm}37.89$ mg/dL, respectively ($P$ < 0.018). Low-density lipoprotein cholesterol was $101.36{\pm}23.57$ mg/dL and $120.60{\pm}34.62$ mg/dL ($P$ < 0.005) in the vegetarians and omnivores, respectively, indicating that vegetarians had significantly lower lipid levels. Thus, oxidative stress, body fat, and cholesterol levels were lower in long-term vegetarians than those in omnivores.
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