Cataracts are the leading cause of blindness worldwide and are characterized by increased opacity of the lens that significantly diminishes visual acuity. It has been suggested that increased risk of lens opacities are associated with age, exposure to sunlight, diabetes, smoking, and poor nutrition. Antioxidant nutrients have born demonstrated to protect the lens membrane and protein against damage due to oxidative stress. The purpose of this study was to investigate the antioxidant system in the blood of cataract patients. The status of the blood antioxidant system was evaluated based on the levels of antioxidant vitamins and minerals as well as glutathione peroxidase (GSH-Px) and malondialdehyde (M7A) activity in 34 patients with cataracts (17 male and 17 female) and 45 control subjects (20 male and 25 female). After adjusting for age, the results showed significantly lower levels of antioxidant vitamins such as lycopene (M : p < 0.05, F: p < 0.01), zeaxanthin (F: p < 0.01), ${\gamma}$-tocopherol (F: p < 0.01) and ascorbic arid (M: p < 0.05) in the cataract patients than in the control subjects. In contrast, the concentration of cryptoxanthin (F : p < 0.07) showed a significantly higher value in the cataract patients. The serum level of the antioxidant mineral Zn (M : p < 0.01) was found to be significantly lower in the cataract patients while the ratio of cu/zn appeared significantly higher (M : p < 0.05). Significantly higher (M : p < 0.01, F: p < 0.05) concentrations of MDA in serum was found in the cataract patients as compared to the control subjects. GSH-Px activity was significantly lower (F: p < 0.05) in 71e cataract patients. In conclusion, the antioxidant system may play an important roll in cataract creation. Further studies are needed to clarify the mechanisms underlying these findings and to establish preventive measures with an emphasis on antioxidant nutrition for cataract patients.
An adaptive measure of photosynthetic cells to a condition identified with a reduction of cellular energy charge, caused by water deficit-induced impairment of photosynthetic ATP production, was investigated using hydroponically cultured rice seedlings. Water stress treatment of the seedlings resulted in a marked decrease in cellular ATP level, a significant increase in the content of NAD(H) and concurrent decrease in that of NADP(H) in shoots, which accompanied a decrease in the activity of NAD kinase (EC 2.7.1.23) that specifically converts NAD(H) to NADP(H). The decline in the enzyme activity was particularly evident in the $Ca^{2+}/calmodulin-dependent$ kinase, the major form of NAD kinase in plants, whereas the level of active calmodulin remained unchanged during water deficit. The ratio of $NADP^+$ to NADPH was maintained nearly constant and no increases were seen in the level of $H_2O_2$ and the activities of $superoxide/H_2O_2-detoxifying$ enzymes in shoots stress-treated for two days. Based on these results, it may be suggested that rice plants take a strategy to cope with an adverse situation of limited photophosphorylation created by water deficit in that cells facilitate ATP production through glycolysis and oxidative phosphorylation; in doing so, rice cells suppress NAD kinase activity, consequently up-sizing the NAD(H) pool at the expense of the NADP(H) pool. Several parameters associated with the stress symptoms are also of implicative that there is no overproduction of superoxide radical or the related active oxygen at least in rice seedlings.
An experiment was carried out with 48 IVRI 2CQ rats 6-8 week old, weighing 50-100 g, to study the effect of lead exposure on antioxidant defense, lipid peroxide level, status of thiol groups and concentration of lead in the liver and kidneys at the end of the exposure and also after withdrawal of lead administration. Twenty four rats were given lead at a daily dose rate of 1 mg lead/2 ml of distilled water/kg body weight as lead acetate solution intraperitoneally for a period of 30 days. Another 24 control rats received 2 ml of sterile normal saline solution (0.85% NaCl)/kg body weight in an identical manner. A many-fold increase in concentration of lead was associated with a non-significant (p>0.05) decrease in the activities of superoxide dismutase (SOD) in the liver (27%) and kidneys (12%) and catalase in kidneys (22%). A significant (p<0.05) increase in lipid peroxide level was recorded in the liver (40%) compared with control values. There were significant (p<0.05) decreases in the total thiol and protein bound thiol contents in liver and an increase in non-protein bound thiol groups in the kidneys of lead exposed rats. During the 10 day observation period after withdrawal of lead administration, no significant change was observed with respect to any of the above parameters indicating that a 10 day withdrawal period was not enough for restoration of normality. It is concluded that the magnitude of response and the resultant changes in the lipid peroxide concentration, and the activities of SOD and catalase were not identical in the liver and kidneys of lead-exposed rats.
Inflammatory bowel disease (IBD) is an increasing global burden and a predisposing factor to colorectal cancer. Although a number of treatment options are available, the side effects could be considerable. Studies on fecal microbiota transplantation (FMT) as an IBD intervention protocol require further validation as the underlying mechanisms for its attenuating effects remain unclear. This study aims to demonstrate the ameliorative role of FMT in an ulcerative colitis (UC) model induced by dextran sulfate sodium (DSS) and elucidate its relative mechanisms in a mouse model. It was shown that FMT intervention decreased disease activity index (DAI) levels and increased the body weight, colon weight and colon length of experimental animals. It also alleviated histopathological changes, reduced key cytokine expression and oxidative status in the colon. A down-regulated expression level of genes associated with NF-κB signaling pathway was also observed. The results of 16S rRNA gene sequencing showed that FMT intervention restored the gut microbiota to the pattern of the control group by increasing the relative abundance of Firmicutes and decreasing the abundances of Bacteroidetes and Proteobacteria. The relative abundances of the genera Lactobacillus, Butyricicoccus, Lachnoclostridium, Olsenella and Odoribacter were upregulated but Helicobacter, Bacteroides and Clostridium were reduced after FMT administration. Furthermore, FMT administration elevated the concentrations of SCFAs in the colon. In conclusion, FMT intervention could be suitable for UC control, but further validations via clinical trials are recommended.
The objective of this study was to determine the effect of genotype (slower-growing vs. fast-growing) and production system (access to outdoors vs. indoor) on the growth performance, carcass yield and meat quality (chemical composition, physicochemical and sensory properties) of chickens. The experiment was performed on 1,040 day-old hybrid male chickens of two genotypes. Slower-growing chickens (Hubbard JA957, certified) and fast-growing chickens (Hubbard F15) were fed identical diets until 65 days of age. Both genotypes (each represented by 520 birds) were divided into two subgroups and were raised in pens on litter with outdoor access or in indoor confinement without outdoor access (four replications per subgroup, each of 65 birds). Until day 21, the birds stayed in the indoor facility, in deep-litter pens. The birds could forage on pasture 12 h daily, commencing at three weeks of age. Stocking density was 0.13 $m^2$ floor space per bird in pens on litter, and 0.8 $m^2$ per bird in grassy yards. Compared with fast-growing, slower-growing chickens were significantly lighter (by 17%), had a lower breast and thigh muscle yield and a higher abdominal fat content, but they were characterized by higher survival rates at 65 days, a higher protein content and a lower fat content of breast meat. Outdoor access had no negative effects on the growth performance, muscle yield, the fatty acid profile and oxidative status of meat lipids. The meat of free-range chickens was darker in color, it had a higher protein content and a better water-holding capacity, but it was less juicy than the meat of birds raised indoors.
Kim, Kyung-Ja;Lee, Hye-Jin;Park, Yoo-Kyoung;Kang, Myung-Hee
Journal of Nutrition and Health
/
v.39
no.8
/
pp.773-785
/
2006
Vitamin E in the body system plays an important role in preventing chronic diseases by decreasing the oxidative stress by free-radicals. However, there are not enough researches on analyzing the primary factors affecting vitamin E levels in the blood in Korean adults. Therefore, the purpose of this research was to examine blood tocopherol levels and the primary factors affecting the status. A complete lifestyle survey was performed on 314 Korean adult men and surveyed their smoking, drinking and exercising habits. The average plasma level of ${\alpha}-\;and\;{\gamma}-tocopherol$ showed similar mutual relations with plasma total cholesterol (TC), triglyceride (TG), or low density lipoprotein cholesterol (LDL-C) levels (p<0.001). Plasma ${\alpha}-tocopherol$ level of the subjects did not show any difference as smoking, drinking and exercising habits changed. However, ${\gamma}-tocopherol$ per TG showed much lower figure in smokers than non smokers (p < 0.05). Amongst diet factors, plasma ${\alpha}-tocopherol$ level showed negative correlations with Vitamin E intake, while ${\gamma}-tocopherol$ level showed positive correlations with Vitamin E intake. Erythrocyte superoxide dismutase (SOD) activity and plasma tocopherol showed negative correlations, and catalase activity and plasma ${\alpha}-tocopherol$ showed positive correlationship. The level of cell DNA damage of Iymphocyte and plasma ${\alpha}-\;or\;{\gamma}-tocopherol$ showed negative correlations. As a result of this research, the factors that affect Korean adult men's plasma ${\alpha}-tocopherol$ level are plasma TG, LDL-C and cell DNA damage in Iymphocyte, while the factors that affect ${\gamma}-tocopherol$ level are plasma TG, LDL-C and vitamin E intake based on multiple regression analysis. These findings implies that the level of different types of tocopherol depends on slightly different factors. A further research is needed on the factors involved in the differentiation of the types of tocopherol.
Few studies have shown the correlation between metabolic syndrome and bone mineral density (BMD). The main pathogenic mechanisms of metabolic syndrome rely on chronic low-level inflammatory status and oxidative stress. There are few studies that examine the gender-specific effects of inflammation and antioxidants on BMD. In this study, we evaluated the relative contribution of these factors in patients with metabolic syndrome. We conducted a cross-sectional study of 67 men and 46 postmenopausal women with metabolic syndrome; metabolic syndrome was defined as having three or more metabolic syndrome risk factors. BMD, body fat mass, and lean body mass were evaluated. We also examined the levels of high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), adiponectin, vitamin E, and C in serum. Log-transformed hs-CRP levels were significantly higher in lumbar spine osteoporotic subjects than in normal subjects for women but not for men. There was no significant difference between the normal group and the osteoporotic group in other inflammatory markers. Stepwise regression analyses for BMD of the lumbar spine showed that lean body mass and vitamin E were significant determinants in men. Lean body mass and log-transformed hs-CRP were significant determinants in women Analysis for BMD of the femoral neck showed that lean body mass was a significant determinant for both men and women. There was no significant factor among the inflammatory markers or antioxidant vitamins affecting the femoral neck BMD for either gender. In conclusion, while hs-CRP is an independent predictor of the BMD of the lumbar spine in women, vitamin E showed profound effects on BMD in men but not women with metabolic syndrome.
It has been reported that cigarette smoking increases free radical generation, which can also increase lipid peroxides and deplete antioxidants. The purpose of this study was to determine whether cigarette smoking and other lifestyle choices may affect serum lipid peroxide concentrations, serum antioxidant concentrations such as tocopherol and vitamin C, and serum antioxidant enzyme activity such as glutathione peroxidase and superoxide dismutase. Dietary intakes were assessed by 24-hour recall and survey questionnaires from 48 male non-smokers and 52 male smokers. Overnight fasting blood was collected and measured for individual antioxidant status. The daily vitamin C intakes of smokers tended to be lower than those of non-smokers, and the intakes of both groups were under the Recommended Daily Allowance (RDA). Vitamin E intake was sufficient for smokers and non-smokers. Serum lipid peroxide concentrations were no difference among all subjects. The serum $\alpha$-tocopherol concentrations of all subjects were in a normal range, and they were highest in mild smokers (p<0.05). Mean serum vitamin C levels were lowest in heavy smokers (p<0.05). The activities of serum glutathione peroxidase and superoxide dismutase were not significantly different in smokes and non-smokers. In conclusion, smoking did not increase oxidative stress in heathy young men. However, it is desirable for heavy smokers to consume more vitamin C than the RDA sine their serum vitamin C concentrations are relatively low.
Acrolein, a known toxin in cigarette smoke, is the most abundant electrophilic $\alpha$, $\beta$-unsaturated aldehyde to which humans are exposed in a variety of environmental pollutants, and is also product of lipid peroxidation. Increased unsaturated aldehyde levels and reduced antioxidant status plays a major role in the pathogenesis of various diseases such as diabetes, Alzheimer's and atherosclerosis. The findings reported here show that low concentrations of acrolein induce heme oxygenase-1 (HO-1) expression in RAW 264.7 macrophages. HO-1 induction by acrolein and signal pathways was measured using reverse transcription-polymerase chain reaction, Western blot and immunofluorescence staining analyses. Inhibition of extracellular signal-regulated kinase activity significantly attenuated the induction of HO-1 protein by acrolein, while suppression of Jun N-terminal kinase and p38 activity did not affect induction of HO-1 expression. Moreover, rottlerin, an inhibitor of protein kinase $\delta$, suppressed the upregulation of HO-1 protein production, possibly involving the interaction of NF-E2-related factor 2 (Nrf2), which has a key role as a HO-1 transcription factor. Acrolein elevated the nuclear translocation of Nrf2 in nuclear extraction. The results suggest that RAW 264.7 may protect against acrolein-mediated cellular damage via the upregulation of HO-1, which is an adaptive response to oxidative stress.
Smoking can increase oxidative stress and thereby change the antioxidant defense system in the body. To investigate the relationship between male adolescent smoking and antioxidant status, we surveyed the eating habits and dietary intake of 82 smokers and 44 nonsmokers recruited from a male technical high school. In addition, antioxidant enzyme activity and lipid peroxide values were determined in both the plasma and the erythrocytes. Although the frequency of food intake was not significantly different, most nutrient intake was unexpectedly higher in smokers than in nonsmokers. In comparison with the Korean RDA, especially the average intake of Ca, Fe and vitamin $B_2$ didn t reach 75% of the Korean RDA in either smokers or nonsmokers. An analysis of antioxidant enzyme activity showed that plasma catalase. superoxide dismutase (SOD), glutathione peroxidase (GSH-px), erythrocyte catalase and GSH-px activities showed no significant difference between smokers and nonsmokers. However, the erythrocyte SOD activity of smokers (1.57 unit/mgHb) was significantly lower than that of nonsmokers (2.00 unit/mg Hb). In addition, the plasma ceruloplasmin concentration of smokers (28.68 mg/$d\ell$) was significantly higher than that of nonsmokers (26.30 mg/$d\ell$), whereas the specific ceruloplasmin ferroxidase activity of smokers (0.31 unit/mg) was lower than that of nonsmokers (0.35 unit/mg). The plasma and erythrocyte thlobarbituric acid reactive substance (TBARS) of smokers (2.57 $\mu$mol/L, 0.32 $\mu$mol/gHb) were also significantly higher than those of nonsmokers (2.25 $\mu$mol/L, 0.27 $\mu$mol/gHb). The overall data indicate that adolescent smoking might decrease the antioxidant capacity of the body, in part, by lowering the erythrocyte SOD activity and the specific ceruloplasmin ferroxidase activity.
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