关于血清 Cu,Zn及 CuZn-SOD 与恶性肿瘤关系的探讨

本文用原子吸收光度法,Ｏｙａｎｇｕｉ法及ＡｄａｃｈｉＹ法分别测定了正常人与五种肿瘤患者血清Ｃｕ,Ｚｎ含量,铜锌超氧化物歧化酶（ＣｕＺｎ－ＳＯＤ）的活性以及谷胱甘肽硫转移酶（ＧＳＴ）的活性。结果表明：恶性肿瘤患者血清中铜含量升高,锌含量降低,ＣｕＺｎ－ＳＯＤ活性降低,而ＧＳＴ活性在正常人与肿瘤患者间无显著差异（Ｐ＞０．０５）。提示人血清中高铜,低锌,高铜／锌比值,以及ＣｕＺｎ－ＳＯＤ活性降低与恶性肿瘤的发生有关。     

复合微量元素缓释丸对放牧反刍动物Cu、Co、Se营养价值的研究

从放牧生态环境大群的大别山黄牛和英山白山羊中选择年龄,体重相近的２０头牛和２０头羊,各随机分为两组,每组１０头,雌、雄均匀配,以复合微量元素缓释丸为试验材料,、每Ⅰ组投丸为试验组,每Ⅱ组不投丸为对照组,牛的两组每组以５头补料,５头不补料,试验期１３５ｄ。羊的两组均不补料,为全放牧方式,试验期６０ｄ,试验结束对羊Ⅰ、Ⅱ组各随机抽取３头屠宰,取样测定肝、肾、脾、肌肉、心、血和瘤胃内容物测定Ｃｕ、Ｃｏ和     

Serum trace elements status of rabbits supplemented with Nigella sativa,vitamins C and E,and selenium against damage by N-methyl-N'-nitro-N-nitrosoguanidine

In this study, we investigated the effects of Nigella sativa, vitamins C and E, and selenium on the levels of trace elements in the serum of N-methyl-N′-nitro-N-nitrosoguanidine (MNNG)-injected rabbits. The rabbits were separated into one control and three experimental groups, each consisting of eight rabbits. MNNG was administered to all rabbits at a dose of 20 mg/kg. Group A received a suspension of N. sativa, group B received a combination of vitamins C and E and selenium, and group C received MNNG without any additional treatment. Group D did not receive any treatment and acted as control. The concentrations of serum zinc, copper, and iron were determined for groups A, B, C, and D. The zinc levels were 155.3±25.8, 304.7±14.22, 117.2±27.9, and 87.0±8 μ/dL for groups A-D, respectively; copper was measured at 234.8±31.9, 214.3±14.2, 196.5±19.3, and 359.2±19.9 μ/dL and iron levels were 276.3±10.71, 260.8±7.15, 211.2±13.47, and 223.4±9.5 μ/dL, in the stated group order. There were statistically significant differences between groups (p<0.05). The results obtained in this work may be of use for monitoring and preventing the nocive effects of N-methyl-N′-nitro-N-nitrosoguanidine and similar carcinogens.     

Effects of methionine containing paracetamol formulation on serum vitamins and trace elements in male rats

Methionine is an effective antidote in the treatment of paracetamol-induced toxicity but at large doses it has been reported to induce or aggravate a number of pathological conditions. It also alters plasma levels of many vital elements and molecules. This study was designed to identify if the alteration observed for antioxidant vitamins and minerals especially at sub-toxic and toxic levels of exposure in our earlier study of 24-hour exposure period may warrant trace elements supplementation. This was investigated by carrying out a 48-hour study to test the ability of a living organism to restore homeostasis of these vital molecules and elements. The levels of antioxidant minerals and vitamins were estimated in the serum samples obtained from adult male Wistar rats exposed to paracetamol tablets. At 100 mg\kg BW (body weight) vitamin A, niacin, riboflavin, selenium and manganese were not significantly different from the control group. Moreover at 350 mg\kg, all these indices except zinc were not significantly different in the exposed group compared with controls whereas at 1000 mg\kg level of exposure manganese, selenium and vitamin E were not significantly decreased at the end of 48 hours of exposure but copper, niacin and vitamin A were significantly increased in the exposed group compared with the controls. These results suggest that with time the body may be capable of bringing about restoration of the levels of some of these elements\vitamins. This was more evident at 350 mg\kg level of exposure than a higher dose of 1000 mg\kg level.Keywords: Paracetamol formulation, Vitamins, Trace elements.     

螺旋藻对小鼠SOD和GSH—Px活力的影响

采用微量测定法,观察螺旋藻对３２只昆明种小白鼠全血中超氧化物歧化酶（ＳＯＤ）和谷光甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性的影响。结果表明,灌胃螺旋藻试验组（ＳＯＤ）活性（１５７７．１６±１６９．８８ＩＵ／ｇＨｂ）,与相应对照组（１３３６．２７±１５８．２３ＩＵ／ｇＨｂ）比较,ＧＳＨ－Ｐｘ活性（２８．３３±２．３７ＩＵ／ｍｌ）与相应对照组（２４．８７±３．２６ＩＵ／ｍｌ）比较,差别均有非常显著意义（Ｐ＜０．０１）;提示螺旋藻有提高动物ＳＯＤ和ＧＳＨ－Ｐｘ活性的功效     

Protective antioxidant effect of vitamins C and E in streptozotocin induced diabetic rats

We have investigated the protective effect of vitamin C and E together supplementation on oxidative stress and antioxidant enzyme activities in the liver of streptozotocin-induced diabetic rats, unsupplemented diabetic and control rats. We also determined the levels of both the vitamins and oxidative stress in plasma. Vitamin supplementation in diabetic rats lowered plasma and liver lipid peroxidation, normalised plasma vitamin C levels and raised vitamin E above normal levels. In liver, the activity of glutathione peroxidase was raised significantly and that of glutathione-S-transferase was normalised by vitamin supplementation in diabetic rats. The levels of lipid peroxidation products in plasma and liver of vitamin-supplemented diabetic rats and activities of antioxidant enzymes in liver suggest that these vitamins reduce lipid peroxidation by quenching free radicals.     

Effects of halothane, enflurane, and isoflurane on plasma and erythrocyte antioxidant enzymes and trace elements

Alterations of the normal redox balance in mammals might be attributed to increases of plasma free-radical concentrations and/or a disruption of the protective mechanisms. These conditions lead to damage to cellular structure by the mechanism of lipoperoxidation, particularly in the liver, kidney, and central nervous system. In this study, the effect of general anesthesia on the oxidative metabolism of human plasma and erythrocytes was investigated. Forty-five patients undergoing anesthesia by using halothane, enflurane, or isoflurane were included in this study. Blood samples were taken preoperatively, the first hour, the first day, and the third day after the operation. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and trace elements such as cofactor copper (Cu), zinc (Zn) and selenium (Se) levels were measured in plasma and red blood cells. Our results showed that halothane and enflurane administration increased the plasma GSH-Px activity and reduced zinc levels. In addition, they lowered SOD and GSH-Px activities and trace element levels on erythrocytes. Isoflurane had no effect on plasma antioxidant enzymes, but, similar to the other, isoflurane decreased the plasma zinc levels, erythrocyte SOD and GSH-Px activities and trace element levels. Gülhane Military Medical Academy     

The effects of acute acetaminophen toxicity on hepatic mRNA expression of SOD,CAT, GSH-Px,and levels of peroxynitrite,nitric oxide,reduced glutathione,and malondialdehyde in rabbit

Molecular and Cellular Biochemistry -     

Effects of omeprazole consumption on serum levels of trace elements

ProjectOmeprazole is one of the most frequently prescribed drugs in patients with gastroesophageal reflux disease (GERD). It increases the gastric pH and this in turn may change the intestinal absorption of trace elements. This study was conducted to assess the effects of omeprazole consumption on the serum level of trace elements.ProceduresThe studied subjects were selected from the list of patients referred to the gastroenterology department of 5 Azar hospital in Golestan province of Iran for whom omeprazole was prescribed by a gastroenterologist. Blood samples were obtained before (phase I) and after an eight-week period (phase II) of omeprazole consumption. Serum levels of trace elements were assessed by the photometric method.ResultsSixty seven patients were recruited of whom, 35.82% were males. There was no significant difference in serum levels of Fe, P, Ca and Cu between phases I and II. Serum concentration of Zn was significantly lower in phase II than I (P = 0.02). The proportion of male patients with low Zn levels was significantly higher in phase II (50%) than I (16.7%) (P = 0.01). We found no significant difference in the proportion of female patients with low Zn levels between phase I (37.2%) and phase II (27.9%).ConclusionsWe found no significant reduction in serum levels of Fe, P, Ca and Cu in phase II. However, our results showed that serum level of Zn was significantly lower after omeprazole consumption in males. So, nutritional supplement of Zn should be considered in male patients treated with omeprazole.     

Effects of vitamins A, E, C and P on intensity of blood coagulation in experimental animals]

In experiment on white rats it was shown that preventive 12-day administration of vitamins A, E, C, P decreases the death rate of animals with exogenous thromboplastinemia and reduces hemocoagulative changes, microcirculation disorders, destructive changes of functionally active elements of inner organs. The protective effect of the above vitamins combination in thromboplastinemia is promoted by hypoactivity of platelet aggregation, by low thromboplastic activity of erythrocytes, by limited destruction of vascular endothelium.     

Serum trace elements and fat-soluble vitamins A and E in healthy pre-school children from a Venezuelan rural community.

Zn (SZn), Cu (SCu), Fe (SFe), vitamin A (SVA) and vitamin E (SVE) were measured in blood serum samples of 85 healthy pre-school children aged 2-6 yr. from the rural community of Canaguá, Mérida State, Venezuela. The relationship between these biochemical indexes was also investigated. The mean serum concentrations of zinc, copper, iron, vitamin A and vitamin E were 0.74 +/- 0.25, 1.18 +/- 0.30, 0.76 +/- 0.20, 0.30 +/- 0.15 and 5.87 +/- 0.43 mg/L, respectively. There was a tendency for SZn to increase with age, whereas SCu and SVA decreased. There was no significant difference in serum trace elements and fat-soluble vitamin concentration between males and females in the different age groups. SFe tended to be lower than that reported in the literature. However, the age groups studied showed no statistically significant sex- and age-related differences. The present study shows that there is a complex interaction between SZn, SCu, SFe, SVA, SVE and age of the children. Multiple regression analysis showed serum zinc was strongly related to serum copper, and serum iron. Serum vitamin A was strongly related to serum zinc and serum vitamin E, whereas serum vitamin E was strongly related to serum zinc, serum copper, and serum vitamin A. On the other hand, our observations also suggest that more detailed studies of these metals and fat-soluble vitamins should be carried out, and that the study should include nutritional surveys, metabolic balances and associations between SZn, SCu, SFe, SVA and SVE and anthropometric variables (height, weight, body mass index and skinfold thickness).     

Alterations of trace elements (Zn, Se, Cu, Fe) and related metalloenzymes in rabbit blood after severe trauma

To investigate the status of the trace elements (TEs) and related metalloenzymes activities in the injury and repair process after severe trauma, we established a rabbit model of severe trauma whose Injury Severity Score (ISS) was 22. Concentrations of blood selenium (Se) and serum copper (Cu), zinc (Zn), iron (Fe), and ferritin were measured on D0 (before injury), and day (D) 1, D2, D3, D6, D9, D14, D21, D28 after trauma, respectively. The activities of glutathione peroxidase (GPx), Cu/Zn superoxide dismutase (Cu/Zn-SOD), myeloperoxidase (MPO), the contents of lipid peroxidation product malondialdehyde (MDA) and serum biochemical profile were detected synchronously. In addition, the morphologic changes of major organs were observed at different time intervals. Results showed that blood Se and serum Zn, Fe contents decreased significantly within 2 weeks after injury. Serum Cu concentration was significantly reduced on D1 but normalized quickly. Serum ferritin level increased during the first week while following an obvious decrease thereafter. The blood GPx activity dropped markedly from D1 to D6, the serum Cu/Zn-SOD activity decreased on D1 and then increased significantly within 2 weeks, and the blood MPO-positive stained cells increased within a week after trauma and followed by a decrease from D14 to D21. The serum MDA increased significantly on D6. Seven of 34 rabbits died in 4-6 days after injury. Biochemistry values and pathological features revealed these rabbits died of multiple organ dysfunction syndrome (MODS). Our experiment suggested that the circulating TEs status is dramatically modified in response to trauma, which might be a factor in MODS.     

Topical antioxidant vitamins C and E prevent UVB-radiation-induced peroxidation of eicosapentaenoic acid in pig skin

Eicosapentaenoic acid protects against UV-radiation-induced immunosuppression and photocarcinogenesis, but it is also prone to oxidative degradation, which may reduce or abolish its beneficial effects. The protective effect of topically applied vitamin E, vitamin C, or both against UVB-radiation-induced lipid peroxidation in the presence of eicosapentaenoic acid was investigated using an ex vivo pig skin model. Changes in the bioavailability of both antioxidants induced by UV radiation were studied in different skin compartments. The UVB-radiation dose used (25 kJ/m2) was similar to that required to induce immunosuppression in BALB/c mice. Exposure of pig skin with an epidermal eicosapentaenoic acid content of 1.0 +/- 0.3 mol% to UVB radiation resulted in an 85% increase of epidermal lipid peroxidation (P < 0.005). Topical application of vitamin E or vitamin C 60 min prior to UVB irradiation resulted in a major increase in both antioxidants in the stratum corneum and viable epidermis (P < 0.05). Vitamin E and vitamin C completely protected against UVB-radiation-induced lipid peroxidation (P < 0.005), but compared to vitamin E, a 500-fold higher vitamin C dose was needed. UVB irradiation induced a vitamin E consumption of up to 100% in the stratum corneum and viable epidermis, and a vitamin C consumption of only 21% in the stratum corneum. Simultaneously applied vitamin E and vitamin C also completely protected against UVB-radiation-induced lipid peroxidation (P < 0.05), and lower antioxidant doses were needed compared to vitamin E or vitamin C alone. In the presence of vitamin C, epidermal vitamin E was more stable upon UVB irradiation (P < 0.05), suggesting interaction between vitamin E and vitamin C. In conclusion, topically applied vitamin E and/or vitamin C efficiently protect against UVB-radiation-induced lipid peroxidation in the presence of eicosapentaenoic acid. The beneficial biological effects of eicosapentaenoic acid may therefore be improved if vitamin E and/or vitamin C are present in sufficient amounts. The ex vivo pig skin model provides a useful tool for assessing short-term biochemical effects related to UVB radiation, without the use of living experimental animals.     

Effects of beta-carotene,vitamin C and E on antioxidant status in hyperlipidemic smokers

Smoking can accelerate the consumption of the stored antioxidant vitamins and increase the oxidative stress in the hyperlipidemic patients. The study investigated the effects of combined beta-carotene, vitamin C, and vitamin E on plasma antioxidant levels, erythrocyte antioxidative enzyme activities, and LDL lipid peroxides. Male hyperlipidemic smokers (35-78 years old) were randomly divided into two antioxidant supplemented groups: intervention 1 (I1, n = 22) (15 mg beta-carotene/day, 500 mg vitamin C/day, and 400 mg alpha-tocopherol equivalent/day) and intervention 2 (I2, n = 20) (30 mg beta-carotene/day, 1000 mg vitamin C/day, and 800 mg alpha-tocopherol equivalent/day). After 6-week supplementation, plasma beta-carotene, vitamin C, vitamin E, and erythrocyte glutathione levels increased significantly by 200%, 98%, 129%, and 39%, respectively, in the I1 group, and by 209%, 216%, 197%, and 32%, respectively, in the I2 group. Plasma Fe(+2) concentrations and Fe(+2)/Fe(+3) decreased significantly in both groups. Except erythrocyte glutathione peroxidase activity in the I1 group, erythrocyte catalase, glutathione peroxidase, and superoxide dismutase activities increased significantly in both groups. Lipid peroxides in LDL decreased significantly by 56% and 72% in the I1 and I2 groups, respectively. However, the levels of plasma iron, erythrocyte glutathione, and LDL lipid peroxides, and the activities of erythrocyte antioxidative enzymes did not differ between two groups. In conclusion, combined antioxidant supplements increased plasma antioxidant levels and antioxidative enzyme activities, and lowered LDL lipid peroxides in male hyperlipidemic smokers. Higher dosage of the supplements did not have an additive effect.     

Update on the effects of vitamins A, C, and E and selenium on carcinogenesis

The effects of vitamins A, C, and E and of selenium on carcinogenesis are briefly summarized and updated. These vitamins and minerals were selected because they have been studied extensively in recent years with a variety of carcinogenesis models. The consumption of vitamin A and its precursors (carotenoids) has been negatively correlated with cancer at a number of sites, particularly the lung. Animal investigations on vitamin A involvement in carcinogenesis have generally been of three types: those assessing the effect of vitamin A deficiency, the effect of excess vitamin A, or the effect of supplementation with synthetic analogs of vitamin A. Vitamin A deficiency had no effect on salivary gland carcinogenesis, enhanced urinary bladder, lung, and liver carcinogenesis, and inhibited colon carcinogenesis. Excess of various forms of vitamin A enhanced or inhibited skin tumorigenesis, inhibited mammary carcinogenesis in rats (but not in mice), and carcinogenesis of the forestomach, liver, and urinary bladder (with one model, but not with another), or enhanced or did not influence lung carcinogenesis. Vitamin A analogs have enhanced or inhibited skin tumorigenesis, inhibited salivary gland, mammary, and urinary bladder carcinogenesis, enhanced tracheal and liver carcinogenesis, and either enhanced or inhibited pancreas carcinogenesis, depending upon the model employed. Although retinoids have been shown to inhibit carcinogenesis at many sites, numerous negative studies have been reported and some reports have indicated enhanced carcinogenesis. The most convincing evidence for the involvement of vitamin C in cancer prevention is the ability of ascorbic acid to prevent formation of nitrosamine and of other N-nitroso compounds. In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid. Like vitamin C, vitamin E can inhibit nitrosation. Vitamin E was shown to inhibit skin, cheek pouch, and forestomach carcinogenesis, to enhance or inhibit colon carcinogenesis, and to have no effect on or to inhibit mammary gland carcinogenesis, depending upon the method of vitamin E administration or the level of dietary selenium or dietary fat. Selenium effects on carcinogenesis have been recently reviewed and the present discussion only updates this area by indicating that enhancement of carcinogenesis by dietary selenium supplements has been observed in the liver, pancreas, and skin.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of protein deficiency on liver trace elements and antioxidant activity in carbon tetrachloride-induced liver cirrhosis

In liver cirrhosis, liver tissue becomes progressively substituted by fibrosis, ultimately leading to architectural distortion, liver circulatory changes, and liver failure. Some data support the hypothesis that protein undernutrition may play a role in the development and progression of nonalcoholic liver cirrhosis and that this progression is at least partially mediated by changes in glutathione peroxidase (GPX), superoxide dismutase (SOD), and other antioxidative systems, leading to an increase in lipid peroxidation. We analyzed the effects of protein deficiency on liver Cu, Fe, Zn, Mn, and Se in carbon tetrachloride (CCl₄)-induced liver cirrhosis, the relation of protein undernutrition and these trace elements with the activity of some hepatic antioxidative enzymatic mechanisms, and the relation of all of them with morphological and biochemical changes in 40 male adult Sprague-Dawley rats divided in four groups. Liver cirrhosis was induced by intraperitoneal injection of CCl₄ to 10 rats fed a 2% protein diet and another 10 fed a 18% protein control diet; two further groups included rats without cirrhosis fed the 2% protein and the 18% protein diets. The study period lasted 6 wk. GPX, SOD, and lipid peroxidation products as well as Zn, Cu, Mn, Se, and Fe were determined in liver samples. We found that liver GPX and Se were reduced in the cirrhotic animals, especially in the low-protein-fed ones, protein deficiency, but not cirrhosis, exerting the main effects. A close correlation was found between liver GPX and serum albumin and weight loss and an inverse one among GPX and hepatocyte ballooning, liver fibrosis, and fat, histomorphometrically determined. These results suggest a pathogenetic role of decreased GPX in the progression of liver disease, which may become enhanced by concomitant protein undernutrition. In addition to iron, the levels of which were increased in the malnourished rats, no differences were found regarding the other trace elements, SOD activity, and lipid peroxidation products.     

Plasma and erythrocytes antioxidant status and trace element levels in proteinuric patients with moderate glomerular function.

The objective of the study was to investigate the effect of moderate glomerular dysfunction on oxidative stress. We determined the plasma and erythrocyte malondialdehyde (MDA) levels, as a marker of lipid peroxidation, erythrocyte glutathione (GSH) levels and activities of GSH-Px, GSH Red and SOD as an antioxidant enzymes, and plasma trace element levels containing Fe, Cu and Zn in twenty proteinuric patients (6.8 +/- 5.1 g/day) with moderate glomerular function and in 20 anemic control subjects. We found that the erythrocyte and plasma MDA levels and erythrocyte GSH-Px activities were significantly higher (p < 0.001, p < 0.001, p < 0.001, respectively) and the erythrocyte GSH levels and activities of GSH-Red and SOD activities were significantly lower (p < 0.001, p < 0.001, p < 0.001, respectively) in the patients than in the anemic subjects. Plasma Fe and Zn levels were not to be found significantly different in the patients compared to the anemic subjects. But plasma Cu levels were significantly higher in the patients (p < 0.05) when compared with the levels of anemic subjects. This study was concluded that cellular antioxidant activity decreases in proteinuric patients with moderate glomerular function. This may increase lipid peroxidation reactions by causing oxidative stress in erythrocyte membranes.     

阿特拉津溶液中仙姑弹琴蛙(Rana daunchina)蝌蚪抗氧化酶系活性的变化

本文研究了阿特拉津 5mg/l、 10mg/l、 15mg/l、 2 0mg/l溶液中经 16d处理和 10mg/l、 2 0mg/l、 30mg/l溶液中经 96d处理后仙姑弹琴蛙 (Ranadaunchina)蝌蚪体内超氧化物歧化酶SOD、过氧化氢酶CAT、谷胱甘肽过氧化物酶GSH Px的活性。受试 16d ,阿特拉津处理组SOD活性分别是空白对照 72 0 6 5 5 8u/μg·ml的0 177、 0 316、 0 4 6 7、 0 36 2倍 ;96d ,分别为空白对照 5 2 2 6 0 4 1u/μg·mL的 0 92 8、 0 4 4 0、 0 4 83倍。表明阿特拉津抑制蝌蚪SOD活性。 16d ,阿特拉津 15、 2 0mg/l组CAT活性分别为空白对照的 0 36 9、 0 183倍 ;96d处理 ,阿特拉津 2 0、 30mg/l组蝌蚪CAT活性分别为空白对照组的 0 76 87、 0 72 2倍 ;阿特拉津 2 0、 30mg/l处理96d ,GSH Px活性为空白对照组的 0 0 83、 0 2 2 5倍。表明高浓度阿特拉津抑制CAT、GSH Px活性。     

mRNA expression of antioxidant enzymes (SOD, CAT and GSH-Px) and lipid peroxidative stress in liver of Atlantic salmon (Salmo salar) exposed to hyperoxic water during smoltification

The mRNA levels of three antioxidant genes, Cu/Zn superoxide dismutase (SOD), catalase (CAT) and phospholipid hydroperoxide glutathione peroxidase (GSH-Px), were quantified with real-time qRT-PCR in liver of Atlantic salmon Salmo salar exposed to 80% (normoxia), 105% and 130% O2 saturation for 54 days. The salmon were then translocated and exposed to 90% and 130% O2 saturation for additional 72 days during smoltification. TBARS and vitamin E levels in liver and the levels of oxidized glutathione (GSSG), total glutathione (GSH) and the resulting oxidative stress index (OSI) in blood were quantified as traditional oxidative stress markers. No significant mean normalized expression (MNE) differences of SOD, CAT or GSH-Px were found in liver after hyperoxia exposure at the two sampling times. Significantly decreased OSI was found in smolt exposed to 130% O2 saturation after 126 days (n = 18, P < 0.0001), indicating hyperoxia-induced oxidative stress. No effects were seen on growth, or on the levels of thiobarbituric reactive substances (TBARS) and vitamin E in liver after the exposure experiment. Overall, the mRNA expression of SOD, CAT and GSH-Px in liver related poorly with the hyperoxic exposure regimes, and more knowledge are needed before the expressed levels of these antioxidant genes can be applied as biomarkers of hyperoxia in Atlantic salmon.