Muscle reinnervation in rats treated with vitamin E]

During muscle reinnervation, a transitory phase of polyinnervation occurs. In reinnervated muscles of vitamin E deficient rats, sprouting and polyinnervation are increased with respect to reinnervated controls. In this work, polyinnervation was observed in reinnervated extensor digitorum longus (edl) muscle of rats treated with pharmacological doses of vitamin E. Sciatic nerve was crushed and edl muscle was examined electrophysiologically at 30, 40 and 60 days after denervation. The percentage of polyinnervated cells in controls peaked at 30 days and thus it decreased. In muscles of vitamin E treated rats, the time course of percentage of polyinnervated muscle cells was qualitatively the same, but it was decreased at all times.     

Vegetable oils used as vitamin E vehicle affect the electrical activity of the rat heart

The aim of this study is to define the possible effects of vegetable oils used as vitamin E vehicle on the electrical activity of the rat heart. To test the possible effects of vitamin E vehicles we studied the effect of i.p. injected corn oil, hazelnut oil or peanut oil on the action potential parameters recorded in both papillary and left atrial muscle strips. Four experimental groups were used. The control group was injected (i.p.) with distilled water, while the three remaining groups received injections of corn oil, hazelnut oil, or peanut oil for five weeks (in a dose of 0.4 ml/kg/day--minimum amount of oil in which vitamin E could be dissolved). We used borosilicated (15-20 megaohms) capillary electrodes and intracellular action potentials (AP) were recorded in isolated papillary and left atrium muscle strips. While administration of three different types of vegetable oil had no significant effect on AP parameters of papillary muscle, they significantly prolonged the repolarization phase of AP in atrial strips. These results show that vegetable oils used as vitamin E vehicles may alter the electrical activity of the heart in a tissue-dependent manner. The present data indicate that the possible effect of vegetable oil vehicles should be kept in mind while evaluating the possible effects of in vivo vitamin E administration.     

Elevated levels of a calcium-activated muscle protease in rapidly atrophying muscles from vitamin E-deficient rabbits.

A Ca2+-activated proteolytic enzyme that partially degrades myofibrils was isolated from hind limb muscles of normal rabbits and rabbits undergoing rapid muscle atrophy as a result of vitamin E deficiency. Extractable Ca2+-activated protease activity was 3.6 times higher in muscle tissue from vitamin E-deficient rabbits than from muscle tissue of control rabbits. Ultrastructural studies of muscle from vitamin E-deficient rabbits showed that the Z disk was the first myofibrillar structure to show degradative changes in atrophying muscle. Myofibrils prepared from muscles from vitamin E-deficient rabbits showed partial or complete loss of Z-disk density. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that the amount of troponin-T (37 000 daltons) and alpha-actinin (96 000 daltons) was reduced in myofibrils from atrophying muscle as compared to myofibrils prepared from control muscle. In vitro treatment of purified myofibrils with purified Ca2+-activated proteolytic enzyme produced alterations in myofibrillar ultrastructure that were identical to the initial alterations occurring in myofibrils from atrophying muscle (i.e. weakening and subsequent removal of Z disks). Additonally the electrophoretic banding pattern of Ca2+-activated proteolytic enzyme-treated myofibrils is very similar to that of myofibrils prepared from muscles atrophying as a result of nutritional vitamin E deficiency. The possible role of Ca2+-activated proteolytic enzyme in disassembly and degradation of the myofibril is discussed.     

Elevated muscle vitamin E does not attenuate eccentric exercise-induced muscle injury.

The purpose of this study was to evaluate the effect of elevated muscle vitamin E content on skeletal muscle damage from eccentric exercise. Sixty Sprague-Dawley rats were put on a normal (40 IU vitamin E/kg food) or supplemented (10,000 IU vitamin E/kg food) diet for 5 wk. Injury in soleus muscle was determined using several criteria: reductions in maximal tetanic force and number of intact fibers per square millimeter and elevations in muscle glucose 6-phosphate dehydrogenase activity and plasma creatine kinase activity, either immediately (0 h) or 2 days (48 h) after a downhill walking protocol. Sedentary animals were also tested but did not exercise. Muscle vitamin E levels were significantly elevated (approximately 3- to 4-fold), and susceptibility of the muscles to oxidant stress was decreased, after supplementation. However, vitamin E supplementation did not attenuate injury by any of the criteria employed. Maximal tetanic force decreased approximately 20% at 0 and 48 h after exercise in both groups. The number of intact fibers per square millimeter decreased approximately 30-35% in both groups at 0 and 48 h. Glucose 6-phosphate dehydrogenase activity increased approximately 50-100% in both groups at 48 h, and plasma creatine kinase activity was elevated approximately 2- to 2.5-fold at 0 h in both groups. These findings do not support a major role for free radical damage to muscle membranes in the initiation of injury from eccentric exercise, although they do not disprove free radical involvement in the etiology.     

Effect of dietary vitamin E level on growth, tissue lipid peroxidation, and erythrocyte fragility of transgenic coho salmon, Oncorhynchus kisutch

This study was conducted to investigate the effect of dietary vitamin E concentration on growth performance, iron-catalyzed lipid peroxidation in liver and muscle tissue, and erythrocyte fragility of transgenic growth hormone coho salmon (Oncorhynchus kisutch). Fish were fed one of four isoenergetic and isonitrogenous experimental diets that contained either 11, 29, 50, or 105 IU of vitamin E/kg. Following the 10-week feeding trial, no significant (P>0.05) diet-related differences were detected in growth, whole body proximate composition or erythrocyte fragility. The vitamin E contents of liver and muscle, however, were affected by the dietary treatment. Fish fed diets containing > or =50 IU of vitamin E/kg had significantly increased vitamin E concentrations in their tissues. Iron-catalyzed lipid peroxidation of liver and muscle tissue of fish fed elevated dietary vitamin E (> or =50 IU vitamin E/kg diet) was significantly lower (P<0.05) than that noted for fish fed the diet containing no supplemental vitamin E. The results indicated that changes in tissue lipid peroxidation measurements precede clinical signs of sub-optimal vitamin E intake.     

Vitamin E requirements of juvenile grass shrimp, Penaeus monodon, and effects on non-specific immune responses

A feeding trial was conducted to determine the dietary vitamin E (DL-alpha-tocopheryl acetate, dl-alpha-TOA) requirement and its effect on the non-specific immune responses of juvenile grass shrimp, Penaeus monodon. Purified diets with eight levels (0, 25, 50, 75, 100, 150, 200, 400 mg vitamin E kg diet-1) of supplemental dl-alpha-TOA were fed to P. monodon (mean initial weight 0.29 +/- 0.01 g) for eight weeks. Each diet was fed to three replicate groups of shrimp. Weight gains and total haemocyte count (THC) were higher (P < 0.05) in shrimp fed diets supplemented with 75 and 100 mg vitamin E kg diet-1 than in shrimp fed diets supplemented with 相似文献   

Oxidative status of plasma and muscle in rabbits supplemented with dietary vitamin E

Thirty New Zealand white rabbits, mean weight 2 kg, were divided into three equal groups balanced for body weight and randomly assigned to a diet containing 60 (C), 150 (T1) or 375 (T2) mg/kg of all-rac-alpha-tocopheryl acetate. After 29 days, the animals were slaughtered. alpha-Tocopherol was assayed in muscle (longissimus dorsi) and plasma; triglycerides and cholesterol (total, high density lipoprotein, low density lipoprotein) were analysed in plasma; reactive oxygen metabolites (ROMs) were analysed in serum; and thiobarbituric acid-reactive substances (TBARS) were analysed in muscle. There were no body weight and food intake differences between the groups. The plasma vitamin E and vitamin E:lipid ratio were significantly higher in groups T1 and T2 than in C, but increases were not linearly related to dietary levels. Muscle alpha-tocopherol concentrations in the treated groups were significantly higher than in C, and linearly related (R =.67) to the vitamin E:lipid ratio. ROM and vitamin E levels in blood were inversely related (R =.74), with ROMs significantly lower in the treated groups than in C. The 60-mg/kg dose of C recommended by the National Research Council was unable to control ROM production. Lipid oxidation in muscle was significantly lower in T2 than in the other groups, and TBARS correlated significantly with muscle vitamin E (R =.61) and serum ROM (R =.73). These data suggest that vitamin E supplemented at 375 mg/kg diet can effectively control ROM production and improve muscle lipostability. ROM assay provides a useful indirect estimate of the oxidative status of muscle in vivo.     

Elevated levels of a calcium-activated muscle protease in rapidly atrophying muscles from vitamin E-deficient rabbits

A Ca²⁺-activated proteolytic enzyme ¹ that partially degrades myofibrials was isolated from hind limb muscles of normal rabbits and rabbits undergoing rapid muscle atrophy as a result of vitamin E deficiency. Extractable Ca²⁺-activated protease activity was 3.6 times higher in muscle tissue from vitamin E-deficient rabbits than from muscle tissue of control rabbits. Ultrastructural studies of muscle from vitamin E-deficient rabbits showed that the Z disk was the first myofibrillar structure to show degradative changes in atrophying muscle. Myofibris prepared from muscles vitamin E-deficient rabbits showed partial or complete loss of Z-disk density. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that the amount of troponin-T (37 000 daltons) and α-actinin (96 000 daltons) was reduced in myofibrils from atrophying muscle as compared to myofibrils prepared from control muscle. In vitro treatment of purified myofibrils with purified Ca²⁺-activated proteolytic enzyme produced alterations in myofibrillar ultrastructure that were identical to the initial alterations occuring in myofibrils from atrophying muscle (i.e. weakening and subsequent removal of Z disks). Additionally the electrophoretic banding pattern of Ca²⁺-activated proteolytic enzyme-treated myofibrils is very similar to that of myofibrils prepared from muscles atrophying as a result of nutritional vitamin E deficiency. The possible role of Ca²⁺-activated proteolytic enzyme in disassembly and degradation of the myofibril is discussed.     

Protective role of intraperitoneally administered vitamin E and selenium on the antioxidative defense mechanisms in rats with diabetes induced by streptozotocin

The aim of this work was to determine the protective effects of intraperitoneally administered vitamin E and selenium (as Na₂SeO₃, Se) on the lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and vitamin E levels, glutathione peroxidase (GSH-Px), reduced glutathione (GSH) activities in the plasma, red blood cell (RBC), liver, and muscle of rats with streptozotocin-induced diabetes. Fifty adult male Wistar rats were used and all rats were randomly divided into five groups. The first group was used as a control and the second group as a diabetic control. A placebo was given to first and second groups by injection. The third group was intraperitoneally administered with vitamin E (20 mg over 24 h), the fourth group with Se (0.3 mg over 24 h), and the fifth group with vitamin E and Se combination (COM) (20 mg vitamin E + 0.3 mg Se over 24 h). This administration was done for 25 days and the TBARS, vitamin E, GSH-Px, GSH levels in the plasma, RBC, liver, and muscle samples were determined. The vitamin E level in the plasma and liver was significantly (p < 0.05) higher in the control than in the diabetic control group. Also, the TBARS levels in the RBC, liver, and muscle were significantly (p < 0.05) lower in the control than in the diabetic control group. However, GSH-Px and GSH activities in RBC, liver, and muscle were not statistically different between the control and the diabetic control groups. The vitamin E levels in plasma and liver (p < 0.01 and p < 0.001) and GSH-Px activities (p < 0.01, p < 0.001) in RBC were significantly higher in vitamin E, Se, and COM groups than in both control and diabetic control groups. However, the TBARS levels of RBC, muscle, and liver in vitamin E and Se administered groups were significantly (p < 0.05-p < 0.001, respectively) decreased. These results indicate that intraperitoneally administered vitamin E and Se have significant protective effects on the blood, liver, and muscle against oxidative damage of diabetes. The abstract of this study was presented in Physiological Research 48(Suppl. 1), S99 (1999).     

Effect of antioxidant vitamin supplementation on muscle function after eccentric exercise

This study investigated the effects of antioxidant vitamin supplementation upon muscle contractile function following eccentric exercise and was performed double blind. Twenty-four physically active young subjects ingested either placebo (400 mg; n = 8), vitamin E (400 mg; n=8) or vitamin C (400 mg; n = 8) for 21 days prior to and for 7 days after performing 60 min of box-stepping exercise. Contractile function of the triceps surae was assessed by the measurement of maximal voluntary contraction (MVC) and the ratio of the force generated at 20 Hz and 50 Hz tetanic stimulation before and after eccentric exercise and for 7 days during recovery. Following eccentric exercise, MVC decreased to 75 (4) % [mean (SE); n = 24; P < 0.05] of the preexercise values and the 20/50 Hz ratio of tetanic tension from 0.76 (0.01) to 0.49 (0.03) [mean (SE); n = 24; P<0.05). Compared to the placebo group no significant changes in MVC were observed immediately post-exercise, though recovery of MVC in the first 24 h post-exercise was greater in the group supplemented with vitamin C. The decrease in 20/50 Hz ratio of tetanic tension was significantly less (P < 0.05) post-exercise and in the initial phase of recovery in subjects supplemented with vitamin C but not with vitamin E. These data suggest that prior vitamin C supplementation may exert a protective effect against eccentric exercise-induced muscle damage.     

Effects of Dietary Selenium, Vitamin E, and Their Combination on Growth, Serum Metabolites, and Antioxidant Defense System in Skeletal Muscle of Broilers Under Heat Stress

This experiment was conducted to evaluate the effects of dietary vitamin E, selenium (Se), and a combination of the two, on the performance, serum metabolites and oxidative stability of skeletal muscle of broilers during heat stress. The broilers raised in either a thermoneutral (23.9°C constant) or heat stress (23.9°C to 37°C cycling) environment were assigned to 6 dietary treatments (0, 0.5, or 1 mg/kg Se; 125 and 250 mg/kg vitamin E; or 0.5 mg/kg Se plus 125 mg/kg vitamin E) from 1 to 49 days of age. At the end of the experiment, blood samples were collected from chicks, the chicks sacrificed, and pectoralis superficialis muscle was used for measurement of malondialdehyde (MDA) concentration and enzyme activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD). The heat-stressed chicks consumed less feed, gained less weight, and had higher feed conversion ratio when compared to thermoneutral chicks (P<0.05). Serum concentrations of iron (Fe) and zinc (Zn) were decreased by heat stress (P<0.05), whereas the serum concentrations of copper (Cu), glucose, and uric acid were significantly increased under heat stress (P<0.05). The chicks that received supplemental of vitamin E exhibited significantly higher serum concentrations of Zn (P<0.05) and significantly lower concentrations of Cu, glucose, and uric acid (P<0.05) when exposed to heat stress. Dietary Se also caused a significant decrease in serum glucose, uric acid, and Cu concentrations of heat-stressed broilers (P<0.05), but had no significant effect on Zn concentration (P>0.05). The GPx activity remained relatively constant (P>0.05), though SOD activity and MDA levels in skeletal muscle were enhanced on exposure to heat stress (P<0.05). The heat-stressed chicks that received the combined supplementary level of vitamin E and Se had the lowest concentration of MDA and the highest activity of SOD in the skeletal muscle (P<0.05). Dietary Se also caused a significant increase in enzyme activity of GPx in the skeletal muscle (P<0.05). These results indicate that the derangement of blood parameters and oxidative stability in broilers under heat stress are improved by supplemental vitamin E and Se.     

Vitamin E regulates mitochondrial hydrogen peroxide generation.

The mitochondrial electron transport system consumes more than 85% of all oxygen used by the cells, and up to 5% of the oxygen consumed by mitochondria is converted to superoxide, hydrogen peroxide, and other reactive oxygen species (ROS) under normal physiologic conditions. Disruption of mitochondrial ultrastructure is one of the earliest pathologic events during vitamin E depletion. The present studies were undertaken to test whether a direct link exists between vitamin E and the production of hydrogen peroxide in the mitochondria. In the first experiment, mice were fed a vitamin E-deficient or-sufficient diet for 15 weeks, after which the mitochondria from liver and skeletal muscle were isolated to determine the rates of hydrogen peroxide production. Deprivation of vitamin E resulted in an approximately 5-fold increase of mitochondrial hydrogen peroxide production in skeletal muscle and a 1-fold increase in liver when compared with the vitamin E-supplemented group. To determine whether vitamin E can dose-dependently influence the production of hydrogen peroxide, four groups of male and female rats were fed diets containing 0, 20, 200, or 2000 lU/kg vitamin E for 90 d. Results showed that dietary vitamin E dose-dependently attenuated hydrogen peroxide production in mitochondria isolated from liver and skeletal muscle of male and female rats. Female rats, however, were more profoundly affected by dietary vitamin E than male rats in the suppression of mitochondrial hydrogen peroxide production in both organs studied. These results showed that vitamin E can directly regulate hydrogen peroxide production in mitochondria and suggest that the overproduction of mitochondrial ROS is the first event leading to the tissue damage observed in vitamin E-deficiency syndromes. Data further suggested that by regulating mitochondrial production of ROS, vitamin E modulates the expression and activation of signal transduction pathways and other redox-sensitive biologic modifiers, and thereby delays or prevents degenerative tissue changes.     

The cooperative antioxidant role of glutathione with a lipid-soluble and a water-soluble antioxidant during peroxidation of liposomes initiated in the aqueous phase and in the lipid phase

A study is made of the effect of GSH as a co-antioxidant with vitamin E during free radical chain autoxidation inhibition studies of dilinoleoylphosphatidylcholine (DLPC) liposomes. Oxidations are initiated in the aqueous phase with azobis(2-amidinopropane hydrochloride) and in the bilayer phase of DLPC with azobis(2,4-dimethylvaleronitrile) under known conditions of the rate of free radical chain initiation (Ri). In reactions initiated in the aqueous phase, GSH is not an efficient antioxidant when acting alone; however, in cooperation with vitamin E in the bilayers, it does effect significant extensions of the efficient induction period of vitamin E. Quantitative studies show that GSH "spares" 0.4 molecules of vitamin E in the bilayer/molecule of GSH and therefore terminates approximately 0.8 peroxyl radical chains as a co-antioxidant with vitamin E. In contrast, GSH is not an effective co-antioxidant with an efficient water-soluble antioxidant, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylate (Trolox). GSH spares only 0.08 molecules of Trolox/molecule of GSH during autoxidation initiated in the aqueous phase with azobis(2-amidinopropane hydrochloride). The inhibition rate constant for GSH in trapping aqueous phase peroxyls is at least an order of magnitude less than that of Trolox. When peroxidation is initiated in the bilayer phase of DLPC with azobis(2,4-dimethylvaleronitrile), GSH is not an effective co-antioxidant with either vitamin E in the bilayer or Trolox in the water. Comparatively higher ratios of GSH to E (GSH/E = 50) or Trolox (GSH/Trolox = 30) are required to give significant extensions of the E or Trolox induction periods. GSH is estimated to preserve only approximately one vitamin E or Trolox molecule for a hundred GSH for peroxidations initiated in the DLPC bilayers. From the kinetic studies and GSH decay studies during inhibition periods, it is concluded that GSH does not act synergistically by regenerating ArOH from the phenoxyl, ArO, radical of vitamin E or Trolox. The mode of antioxidant action of GSH is concluded to be that of trapping peroxyl radicals in the aqueous phase and thereby indirectly sparing vitamin E in the bilayer.     

Effects of nicotine and vitamin E on 6-phosphogluconate dehydrogenase activity in some rat tissues in vivo and in vitro

The aim of this study was to investigate whether nicotine affects 6-phosphogluconate dehydrogenase (6PGD) enzyme activity in some rat tissues, and to see the modulatory effects of vitamin E on this effect in vivo. In addition, the effects of nicotine and vitamin E on 6PGD activity were also tested in vitro. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine + vitamin E [75 mg/kg/day, intragastric (i.g.)]; and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. The results of in vivo study showed that nicotine activated the muscle, lungs, and testicular 6PGD enzyme activity but had no effect on heart and liver 6PGD activity. Also, nicotine + vitamin E activated the muscle, testicle, and liver 6PGD enzyme activity, while this combination had no effect on heart, and lungs in vivo. When nicotine is administered with vitamin E the increase in 6PGD enzyme activity in muscle and testicles were lower. On the other hand the increase in 6PGD enzyme activity was eliminated by vitamin E in lungs, while 6PGD enzyme activity was increased by vitamin E, which was not affected by nicotine only. In vitro results correlated well with in vivo experimental results. Our results suggest that vitamin E may favourably increase 6PGD enzyme activity in liver in nicotine treated rats, while it has negligible effects on this enzyme activity in other tissues.     

Abnormalities of lipid metabolism in the vitamin E-deficient monkey

A soybean protein diet was used to induce vitamin E deficiency in rhesus monkeys. The deficient monkeys had reduced triglyceride concentrations in liver and skeletal muscle, but the cholesterol concentration in their skeletal muscle was increased. A constant amount of radioactively labeled (3)H-cholesterol-7alpha-(3)H was fed daily for 48-114 days to control and vitamin E-deficient monkeys to study the relationship between plasma, liver, and skeletal muscle cholesterol. Plasma cholesterol reached constant, maximum specific activity by the 42nd day both in control and in vitamin E-deficient monkeys. In control and previously deficient vitamin E-treated monkeys the specific activity of cholesterol in liver and skeletal muscle was approximately equal to that of plasma. In vitamin E-deficient monkeys the liver cholesterol specific activity was equal to that of plasma cholesterol, but the ratio of skeletal muscle cholesterol specific activity to plasma cholesterol specific activity was reduced. It is concluded from these studies that there is a specific defect(s) in cholesterol metabolism in the skeletal muscle of vitamin E-deficient monkeys.     

Synergistic inhibition of oxidation in dispersed phosphatidylcholine liposomes by a combination of vitamin E and cysteine

Oxidations of soybean phosphatidylcholine liposomes in an aqueous dispersion initiated by free radicals generated initially either in the aqueous phase or in the lipid phase were efficiently suppressed by vitamin E in the membranes. Vitamin E was consumed linearly with time and, when the inhibition period was over the oxidation proceeded rapidly at a rate similar to that in the absence of vitamin E. L-Cysteine was also effective by itself in scavenging radicals in the aqueous region, but it was consumed more rapidly than vitamin E. On the other hand, cysteine could not scavenge the radicals efficiently in a lipid region. Nevertheless, when vitamin E was incorporated into liposomes, the addition of cysteine in the aqueous phase prolonged the inhibition period and it reduced the rate of decay of vitamin E markedly even when the radicals were generated initially in the lipid bilayer. Furthermore, it was found by an electron spin resonance study that chromanoxyl radical disappeared quite rapidly when it was mixed with cysteine and that the spin adduct of cysteine radical was observed in the presence of alpha-(4-pyridyl-N-oxide)-N-tert-butyl nitrone. It was concluded that L-cysteine located in an aqueous region could regenerate vitamin E by reacting with vitamin E radical formed in a lipid region and show a synergistic antioxidant effect, although its efficiency of vitamin E regeneration was lower than that by vitamin C.     

A relative high dose of vitamin E does not attenuate unweighting-induced oxidative stress and ubiquitination in rat skeletal muscle

We previously reported that intragastric administration of cysteine could be beneficial to prevent unweighting-induced ubiquitination and degradation of muscle protein in association with redox regulation [Ikemoto et al., Biol. Chem., 383 (2002), 715-721]. In this study, we investigated whether vitamin E, another potent antioxidative nutrient, also had beneficial effects on the muscle protein catabolism. However, daily intragastric supplementation of 1.5 or 15 mg/rat of alpha-tocopherol did not prevent weight loss of hindlimb skeletal muscle in tail-suspended rats. To elucidate the reason for the non-effectiveness of vitamin E, we further examined concentrations of oxidative stress markers, ubiquitination of muscle proteins and fragmentation of myosin heavy chain in gastrocnemius muscle of rats daily treated with 15 mg of alpha-tocopherol. Unexpectedly, vitamin E increased concentrations of glutathione disulfide and thiobarbituric acid-reactive substance and decreased glutathione level in the muscle, compared with those of vehicle treatment, indicating that vitamin E enhanced unweighting-induced oxidative stress in skeletal muscle. The vitamin E supplementation did not suppress the ubiquitination of muscle proteins and fragmentation of myosin heavy chain caused by tail-suspension. Our results suggest that supplementation of a relative high dose of vitamin E could not inhibit ubiquitin-dependent degradation of muscle protein in tail-suspended rats possibly due to its prooxidant action.     

Antioxidant levels from different Antarctic fish caught around South Georgia Island and Shag Rocks

Antarctic fish have been isolated for over several million years in an environment with a very low and constant temperature and high oxygen concentration. In such conditions the oxidative stress might be an important factor affecting their metabolic adaptive strategies. Activity of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), vitamin E levels and total antioxidant capacity (TRAP) were measured in liver, gill, heart and muscle homogenates of red-blooded (Nototheniidae) and white-blooded (Channichthyidae) Antarctic fish. SOD activity was also measured in blood samples. Gill SOD activity was threefold higher in channichthyids than in nototheniids while CAT and GPx were significantly higher in the gills of channichthyids. The increased SOD activity of channichthyids probably reflects the large PO₂ gradient across their gills. The H₂O₂ produced seems to be preferentially eliminated by diffusion, according to the low levels of CAT and GPx found in the gills of these species. In contrast, blood SOD was about fivefold higher in the latter group, which possesses erythrocytes and thus a much higher oxygen-carrying capacity. CAT activity was always higher in nototheniids except in muscle. However, vitamin E did not show clear differences between families except for the pattern observed in muscle. The higher content of vitamin E in this tissue shown in channichthyids is related to the higher volume density of mitochondria reported for this group, since vitamin E is responsible for preventing membrane lipid peroxidation. Accordingly, TRAP (representative of hydrosoluble antioxidant capacity) was also higher in muscle of channichthyids. This is probably related to the role of ascorbic (a hydrosoluble compound) acid in regenerating vitamin E. Accepted: 4 September 1999     

Vitamin E deficiency and vitamin C supplements: exercise and mitochondrial oxidation

The effects of dietary antioxidant vitamins E and C on exercise endurance capacity and mitochondrial oxidation were investigated in rats. The endurance capacity of both vitamin E-deficient and vitamin C-supplemented, E-deficient rats was significantly (P less than 0.05) lower (38.1 and 33.6%, respectively) than control animals. Compared with the normal and vitamin E-deficient rats, there was a significant (P less than 0.05) increase in the concentration of vitamin C in blood and liver of the vitamin E-deficient, C-supplemented animals. Hence dietary vitamin C supplementation does not prevent the inhibition of exercise endurance capacity or increased hemolysis seen in vitamin E deficiency. The mitochondrial activities for the oxidation of palmitoyl carnitine and alpha-ketoglutarate were significantly (P less than 0.05) decreased by a single bout of exercise in brown adipose tissue but not in muscle, heart, or liver from vitamin C-supplemented, E-deficient groups of rats when compared with the activities in the tissue from the same group of rats killed at rest. Similar results were also seen in brown adipose tissue from vitamin E-deficient rats. The results suggest a tissue-specific role for vitamins E and C in substrate oxidation and show that the poor endurance capacity of vitamin E-deficient rats cannot be attributed to any changes in the mitochondrial activity in skeletal or cardiac muscles. It is also concluded that vitamin C supplementation, at least at the dose employed in the present study, cannot counteract the detrimental effects associated with vitamin E deficiency.