Lipid Peroxidation In Skeletal Muscle Research Articles

Iron accumulation in skeletal muscles of old mice is associated with impaired regeneration after ischaemia-reperfusion damage.

BackgroundOxidative stress is implicated in the insidious loss of muscle mass and strength that occurs with age. However, few studies have investigated the role of iron, which is elevated during ageing, in age‐related muscle wasting and blunted repair after injury. We hypothesized that iron accumulation leads to membrane lipid peroxidation, muscle wasting, increased susceptibility to injury, and impaired muscle regeneration.MethodsTo examine the role of iron in age‐related muscle atrophy, we compared the skeletal muscles of 3‐month‐old with 22‐ to 24‐month‐old 129SvEv FVBM mice. We assessed iron distribution and total elemental iron using laser ablation inductively coupled plasma mass spectrometry and Perls' stain on skeletal muscle cross‐sections. In addition, old mice underwent ischaemia–reperfusion (IR) injury (90 min ischaemia), and muscle regeneration was assessed 14 days after injury. Immunoblotting was used to determine lipid peroxidation (4HNE) and iron‐related proteins. To determine whether muscle iron content can be altered, old mice were treated with deferiprone (DFP) in the drinking water, and we assessed its effects on muscle regeneration after injury.ResultsWe observed a significant increase in total elemental iron (+43%, P < 0.05) and lipid peroxidation (4HNE: +76%, P < 0.05) in tibialis anterior muscles of old mice. Iron was further increased after injury (adult: +81%, old: +135%, P < 0.05) and associated with increased lipid peroxidation (+41%, P < 0.05). Administration of DFP did not impact iron or measures of lipid peroxidation in skeletal muscle or modulate muscle mass. Increased muscle iron concentration and lipid peroxidation were associated with less efficient regeneration, evident from the smaller fibres in cross‐sections of tibialis anterior muscles (−24%, P < 0.05) and an increased percentage of fibres with centralized nuclei (+4124%, P < 0.05) in muscles of old compared with adult mice. Administration of DFP lowered iron after IR injury (PRE: −32%, P < 0.05 and POST: −41%, P < 0.05), but did not translate to structural improvements.ConclusionsMuscles from old mice have increased iron levels, which are associated with increased lipid peroxidation, increased susceptibility to IR injury, and impaired muscle regeneration. Our results suggest that iron is involved in effective muscle regeneration, highlighting the importance of iron homeostasis in muscle atrophy and muscle repair.

Guava leaves extract ameliorates STZ induced diabetes mellitus via activation of PI3K/AKT signaling in skeletal muscle of rats.

Blood glucose homeostasis and insulin signaling pathway regulation take a vital role in the management of diabetes mellitus. Our present was designed to explore the mechanism of the blood homeostasis, regulation of oxidative stress and insulin signaling pathway by guava leaf extract (GLE). Diabetes mellitus was induced in male albino Wistar by streptozotocin (STZ) (Single dose-40 mg/kg b.w.). As an extension STZ rats received GLE (GLE; 200 mg/kg b.w). At the end of the study the lipid peroxidation products, antioxidants, insulin signaling genes were analyzed. Treatment with GLE resulted in decreased plasma and skeletal muscle lipid peroxidation markers, increased antioxidants, and improved insulin signaling genes. GLE treatment helps to maintain blood homeostasis alleviates oxidative stress and regulates the insulin signaling genes in skeletal muscle. Overall the results suggest GLE treatment regulates blood glucose, inhibits oxidative stress, and importantly it regulates insulin signaling pathway genes in skeletal muscle. Further studies on the GLE role in other important pathways can add additional strength to the claim that GLE is a strong anti-diabetic candidate.

Effects of astaxanthin-rich dried cell powder from Paracoccus carotinifaciens on carotenoid composition and lipid peroxidation in skeletal muscle of broiler chickens under thermo-neutral or realistic high temperature conditions.

Thirty‐two 15‐day old broiler chicks (Chunky strain ROSS 308) were randomly divided into four treatments in a 2 × 2 factorial design. The main factors were diet (basal diet or basal diet supplemented with 0.15% astaxanthin‐rich dried cell powder (Panaferd‐P [astaxanthin 30 ppm]) and ambient temperature (thermo‐neutral [25 ± 1°C] or high [35 ± 1°C for 6 hr]). Dietary supplementation with Panaferd‐P did not affect growth performance, though high ambient temperature decreased feed intake and the weight of breast tender muscle, liver, and heart. High ambient temperature also decreased redness in both breast and leg muscles of chickens, while Panaferd‐P increased redness and yellowness of breast and leg muscles of chickens. Panaferd‐P increased Paracoccus carotinifaciens‐derived pigments (i.e., adonixanthin, astaxanthin, adonirubin, and cantaxanthin) as well as corn‐derived pigments such as zeaxanthin and lutein in breast and leg muscles. High ambient temperature increased the malondialdehyde (MDA) concentration in breast muscle, while Panaferd‐P decreased the MDA concentration in breast muscle under both temperature conditions. Our results suggest that dietary supplementation with Panaferd‐P increases muscle carotenoid content, the redness and yellowness of meat and decreases the muscle MDA concentration in broiler chickens kept under thermo‐neutral or high ambient temperature conditions.

Cardiometabolic response of juvenile rainbow trout exposed to dietary selenomethionine

Selenium (Se) is considered an essential trace element, involved in important physiological and metabolic functions for all vertebrate species. Fish require dietary concentrations of 0.1–0.5 μg Se/g dry mass (d.m.) to maintain normal physiological and selenoprotein function, however concentrations exceeding 3 μg/g d.m. have been shown to cause toxicity. As Se is reported to have a narrow margin between essentiality and toxicity, there is growing concern surrounding the adverse effects of elevated Se exposure caused by anthropogenic activities. Previous studies have reported that elevated dietary exposure of fish to selenomethionine (Se-Met) can cause significant cardiotoxicity and alter aerobic metabolic capacity, energy homeostasis and swimming performance. The goal of this study aims to further investigate mechanisms of sublethal Se-Met toxicity, particularly potential underlying cardiovascular and metabolic implications of chronic exposure to environmentally relevant concentrations of dietary Se-Met in juvenile rainbow trout (Oncorhynchus mykiss). Juvenile rainbow trout were fed either control food (1.3 μg Se/g d.m.) or Se-Met spiked food (6.4, 15.8 or 47.8 μg Se/g d.m.) for 60 d at 3% body weight per day. Following exposure, ultrahigh resolution B-mode and Doppler ultrasound was used to characterize cardiac function in vivo. Chronic dietary exposure to Se-Met significantly increased stroke volume, cardiac output, and ejection fraction. Fish fed with Se-Met spiked food had elevated liver glycogen and triglyceride stores, suggesting impaired energy homeostasis. Exposure to Se-Met significantly decreased mRNA abundance of citrate synthase (CS) in liver and serpin peptidase inhibitor, clad H1 (SERPINH) in heart, and increased mRNA abundance of sarcoplasmic reticulum calcium ATPase (SERCA) and key cardiac remodelling enzyme matrix metalloproteinase 9 (MMP9) in heart. Taken together, these responses are consistent with a compensatory cardiac response to increased susceptibility to oxidative stress, namely a decrease in ventricular stiffness and improved cardiac function. These cardiac alterations in trout hearts were linked to metabolic disruption in other major metabolic tissues (liver and skeletal muscle), impaired glucose tolerance with increased levels of the toxic glucose metabolite, methylglyoxal, increased lipid peroxidation in skeletal muscle, development of cataracts and prolonged feeding behaviour, indicative of visual impairment. Therefore, although juvenile rainbow trout hearts were apparently able to functionally compensate for adverse metabolic and anti-oxidant changes after chronic dietary exposure Se-Met, complications associated with hyperglycemia in mammalian species were evident and would threaten survival of juvenile and adult fish.

Effects of trehalose supplementation on the growth performance and intestinal innate immunity of juvenile chicks

Trehalose is composed of two molecules of D-glucose joined by an α,α-1,1 glucosidic linkage and has antioxidative and anti-inflammatory effects. The present study investigated the effect of feeding a trehalose-supplemented diet on the growth performance, as well as the oxidative status and the intestinal innate immunity of juvenile chicks.A total of 16 d-old male broiler chicks were used in this study: two groups of 8 birds were fed on a 0% (control) or 0.5% trehalose-supplemented diet for 18 d.The mean body weight of the trehalose group was significantly greater than that of the control group, but feed efficiency was not altered by feeding the trehalose-supplemented diet. No differences in the levels of lipid peroxidation in skeletal muscle, liver and plasma were observed between the control and trehalose-supplemented groups. The mRNA levels of interferon-γ, tumour necrosis factor-like ligand 1A, interleukin-10, NADPH oxidase 4 and inducible NO synthase were significantly reduced by the trehalose supplementation.Our results suggest that dietary supplementation with trehalose after hatching may have beneficial effects on the growth performance of juvenile chicks, probably by improving their intestinal innate immunity.

L-glutamine And L-alanine attenuate oxidative stress In Rats Submitted To Heavy Resistance Training

PURPOSE: Determine the effects of oral chronic supplementation with L-glutamine and L-alanine, both in its free form or as dipeptide on gluthatione concentration and lipid peroxidation in rats submitted to heavy resistance training METHODS: Adult male Wistar rats were submitted to resistance training for 6 weeks and supplemented with L-alanyl-L-glutamine (DIP, group), L-glutamine and L-alanine, both in its free form (GLN+ALA, group), L-alanine only (ALA, group) or water (CTRL, group). Resistance training consisted to climb a ladder 3 to 6 sets with progressive loads (25% to 100% of body weight). In the last 21 days of training, supplements were given in a 4% solution dissolved in drinking water. Reduced (GSH) and oxidized (GSSG) gluthatione (mmol/g fresh tissue) GSSG/GSH ratio and TBARS (nmol/mg fresh tissue) were determined in liver and extensor digitorum longus (EDL) muscle. The results were evaluated through the one-way ANOVA and Tukey’s test, with a significance level of 5%. RESULTS: In EDL muscle, a significantly increase of GSH concentration was observed in ALA (0.47±0.05) GLN+ALA (0.50±0.03) and DIP(0.52±0.04) groups compared to CTRL (0.32±0.03). Hence GSSG/GSH ratio (0.054±0.008; 0.038±0.003; 0.039±0.004, respectively) was lower than CTRL (0.091±0.01) (p<0.05). Skeletal muscle lipid peroxidation decreased in ALA (5.0±0.8), GLN+ALA (5.2±0.6) and DIP (4.1±0.8) groups when compared to CTRL (8.26± 0.60) (p<0.05). Liver GSH concentrations were also improved in GLN+ALA (2.85±0.34) and DIP (2.93±0.23) groups compared to CTRL (1,73±0,19). GSSG/GSH ratio decreased in these groups by 34% and 39%, respectively (p<0.05). Liver lipid peroxidation was significantly reduced in GLN+ALA (26%) and DIP (36%) compared to CTRL. CONCLUSIONS: L-glutamine and L-alanine both free or as dipeptide improve glutathione concentration, consequently enhance the redox state and attenuate oxidative stress induced at heavy resistance training. ACKNOWLEDGEMENT: FAPESP

Treadmill Training But Not Resistance Training Protects Against Doxorubicin-induced Skeletal Muscle Lipid Peroxidation

Treadmill Training But Not Resistance Training Protects Against Doxorubicin-induced Skeletal Muscle Lipid Peroxidation

Effects of Feeding Dried Concentrated Rice-Washing Water on Growth Performance and Skeletal Muscle Lipid Peroxidation in Broiler Chickens

This study was conducted to examine the effect of feeding concentrated rice-washing water (CRWW) on growth performance and lipid peroxidation levels in broiler chickens. CRWW (89.8% moisture) was dried at either a high (130°C) or low temperature (60°C). Three experimental diets were formulated as follows: 1) control diet; 2) diet containing 20% high-temperature dried CRWW (HT-CRWW); and 3) diet containing 20% low-temperature dried CRWW (LT-CRWW). Twenty-one chicks were divided into a control group and two treatment groups (seven chicks per group) at 15 days of age. The control group was fed the control diet, and the treatment groups were fed either an HT-CRWW or LT-CRWW-containing diet for 12 days. The growth performance (body weight, weight gain, feed intake, and feed efficiency) and the weight of the pectoral muscles were not different between treatment groups. Both HT-CRWW and LT-CRWW had a higher total polyphenol content and free radical scavenging activity than corn meal. Malondialdehyde (MDA) content, a marker of lipid peroxidation, was significantly lower in the skeletal muscle of chicks fed the HT-CRWW-containing diet compared with chicks fed the control diet; however, MDA content in chicks fed the LT-CRWW-containing diet did not differ from that of controls. CRWW has promise as a high-energy feed resource, and CRWW dried at high temperatures might affect lipid peroxidation in broiler chickens through higher antioxidant activity.

Skeletal Muscle Lipid Peroxidation and Insulin Resistance in Humans

The relationships among skeletal muscle lipid peroxidation, intramyocellular lipid content (IMCL), and insulin sensitivity were evaluated in nine insulin-sensitive (IS), 13 insulin-resistant (IR), and 10 adults with type 2 diabetes (T2DM). Insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp [glucose disposal rate (GDR)]. Lipid peroxidation was assessed by 4-hydroxynonenal (HNE)-protein adducts and general oxidative stress by protein carbonyl content. All patients were sedentary. Protein-HNE adducts were elevated 1.6-fold in T2DM compared with IS adults, whereas IR showed intermediate levels of HNE-modified proteins. Protein-HNE adducts correlated with GDR, waist circumference, and body mass index. IMCL was increased by 4.0- and 1.9-fold in T2DM and IR patients, respectively, compared with IS, and was correlated with GDR and waist circumference but not BMI. Protein carbonyls were not different among groups and did not correlate with any of the measured variables. Correlations were detected between IMCL and protein-HNE. Our data show for the first time that skeletal muscle protein-HNE adducts are related to the severity of insulin resistance in sedentary adults. These results suggest that muscle lipid peroxidation could be involved in the development of insulin resistance.

Trypanosoma evansi: Ca2+ ATPase activity and lipid peroxidation in skeletal muscle from rats experimentally infected

The aim of this study was to evaluate Ca2+ ATPase activity and the lipid peroxidation in muscles from rats experimentally infected by Trypanosoma evansi and its roles in the muscle pathogenesis in trypanosomosis. Thirty-six rats were divided in two groups. Group A was infected with an isolate from T. evansi and group B was used as a negative control. Group A was divided into three subgroups (A1, A2 and A3), three animals each group, as well as group B (B1, B2 and B3). The collection of samples were performed at days 5 (A1 and B1), 15 (A2 and B2) and 30 (A3 and B3) post-infection (PI) with the purpose of comparison between healthy and infected rats in the course of the disease. The Ca2+ ATPase enzyme activity was determined in skeletal muscle samples. Muscle tissue lipid peroxidation was determined by TBARS levels, and histopathologically it was investigated a possible damage to the muscle tissue of rats infected with T. evansi. It was observed a significant decrease of Ca2+ ATPase activity in infected rats compared to not-infected. This enzymatic inhibition was observed at days 5, 15 and 30 PI. A significant increase was observed for TBARS levels in the muscles of infected rats at days 5, 15 and 30 PI. It was not identified any histological alterations for gastrocnemius in rats infected by T. evansi at days 5 and 15 PI. Nevertheless, at day 30 PI it was verified inflammatory infiltrate with mononuclear cells between muscle fibers in three infected rats (50%). T. evansi infections in rats showed a negative correlation between Ca2+ ATPase and TBARS levels. Based on these results we suggest that the leg weakness and muscle injuries common in infected animals with T. evansi may be related to a reduced activity of Ca2+ ATPase and oxidative stress.

Skeletal muscle HNE is related to insulin resistance in sedentary individuals

The relationships among skeletal muscle lipid peroxidation (HNE), intramyocellular lipid content (IMCL), and insulin sensitivity were studied in sedentary adults. We assessed IMCL, glucose uptake (GDR), homeostasis model assessment index (HOMA), BMI, body fat (DXA), waist girth (WAIST), and skeletal muscle HNE adducts in 9 insulin‐sensitive (IS), 13 insulin‐resistant (IR), and 10 adults with type 2 diabetes (DB).GDR and HOMA differed among IS, IR, and DB (GDR: 16.6 ±2.6, 9.3 ± 1.6, 6.6 ± 2.1, p &lt; 0.01; HOMA: 2.0 ± 0.7, 5.2 ± 3.7, 7.0 ± 5.1, p &lt; 0.05. HNE was higher in DB than IS (971 ± 436 vs. 609 ± 170; p &lt; 0.05) and correlated with GDR (R = −0.43, p &lt; 0.05), HOMA (R = 0.43, p &lt; 0.05), and BMI (R = 0.42, p &lt; 0.05), but not with IMCL, WAIST, or DXA. IMCL was higher in DB than in IS and IR (8.1 ± 3.8 vs. 2.0 ± 1.0 and 3.8 ± 2.8, p &lt; 0.01) and correlated with GDR (R = −0.56, p &lt; 0.01). IMCL was the primary predictor of GDR (R2 = 0.31, p &lt; 0.01), while HNE was that of HOMA (R2 = 0.18, p &lt; 0.05).Our data show that (1) skeletal muscle HNE and IMCL are both determinants of the severity of insulin resistance assessed by hyperinsulinemic clamp or HOMA in sedentary adults; (2) HNE and IMCL are not related and thus impact GDR independently. These results reveal, for the first time, a negative relationship between skeletal muscle HNE and insulin sensitivity in sedentary individuals and underscore the importance of lipid peroxidation in insulin resistance.Funded by NIH (DK‐038764, HL‐055782), Department of Veterans Affairs (Merit Review), and Gatorade Sport Science Institute's Student Grant Program.

Vitamin E supplementation alleviates the oxidative stress induced by dexamethasone treatment and improves meat quality in broiler chickens

In the present study, the effects of long-term exogenous glucocorticoids administration and dietary supplementation of alpha-tocopheryl acetate on the induction of lipid peroxidation in skeletal muscle were investigated. Male broiler chicks were randomly assigned to 2 diet treatments: the basal diet supplemented with 20 (low level of vitamin E) or 200 (high level of vitamin E) mg of vitamin E (as DL-alpha-tocopheryl acetate)/kg of diet. At 35 d of age, the chickens in each dietary treatment were randomly divided into 3 groups of 30 chickens and subjected to the following treatments: daily s.c. injection of dexamethasone (DEX, 2 mg/kg of BW) for 6 d, sham injection of saline (control), or the sham-treated pair-fed control that maintained the same feed intake as DEX treatment (pair-control). The results showed that the growth of chickens was suppressed by DEX, whereas it was improved by the high level of vitamin E treatment. The DEX treatment resulted in augmented plasma concentrations of TBA reacting substances. Muscle TBA reacting substances levels were higher in DEX chickens at both 24- and 48-h time points postslaughter. Vitamin E supplementation suppressed the formation of lipid peroxidation in both plasma and skeletal muscle tissues. Muscle activity of superoxide dismutase was significantly increased by DEX treatment in both musculus pectoralis major and musculus biceps femoris and maintained as such during the initial 48 h postmortem. The result of the present study indicated that DEX treatment increased the saturation level of skeletal muscle fatty acids. These results suggest that vitamin E supplementation was favorable for the performance of broiler chickens by alleviating the oxidative stress induced by DEX treatment.

Corticosterone administration induces oxidative injury in skeletal muscle of broiler chickens

The present study had been conducted to explore the effect of corticosterone (CORT) on the induction of lipid peroxidation in skeletal muscle. The experimental chickens were subjected to 1 single s.c. injection of CORT (4 mg/kg of BW). Blood samples were obtained at the beginning and end of a 3-h experimental period. Muscle samples were obtained from musculus pectoralis major and musculus biceps femoris (BF) before and immediately after slaughter, and at 24- and 48-h time points postmortem. The result showed that plasma level of TBA reacting substances (TBARS) was significantly increased, whereas the activity of super-oxide dismutase was decreased after CORT injection. Plasma level of total antioxidant power, as reflected by the ferric reducing-antioxidant power, was increased by CORT administration. The preslaughter level of TBARS could be increased by CORT administration in pectoralis major. In contrast, although the preslaughter level of TBARS was not significantly changed by CORT administration in BF, the augmented TBARS level was detected at 48 h postmortem in BF of CORT chickens. During the period of storage, the concentrations of TBARS increased, whereas ferric reducing-antioxidant power level decreased over time regardless of treatment. In conclusion, the data suggest that elevated CORT due to preslaughter stress would affect the redox balance in skeletal muscle. The result suggested that the oxidative stability during storage of meat is associated with the alteration in muscle physiology induced by CORT administration.

The combination of α-lipoic acid supplementation and aerobic exercise inhibits lipid peroxidation in rat skeletal muscles

We investigated the effect of DL-alpha-lipoic acid (LA) supplementation and regular aerobic exercise on the concentrations of malondialdehyde (MDA) and vitamin E, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and the levels of glutathione (GSH) in rat skeletal muscles (soleus and red gastrocnemius). For 8 weeks, rats (n = 7 per group) were (1) exercised on a treadmill for 30 min d(-1), (2) treated with supplemental LA, or (3) exercised and treated with supplemental LA. Control rats (n = 7) did not receive LA and were not exercised. DL-alpha-lipoic acid (100 mg kg(-1)) was administered daily as an oral supplement. The rats were exercised in a graded manner for 5 d wk(-1). The concentration of MDA in the soleus and red gastrocnemius was significantly lower in rats that exercised and received LA than in the other groups. Compared with the other groups, rats that exercised and received LA had a significantly higher vitamin E concentration in the soleus. The SOD and GPx activities in the soleus and red gastrocnemius were significantly higher in rats that exercised and received LA. These results suggest that LA supplementation combined with aerobic treadmill exercise inhibits lipid peroxidation in skeletal muscles. This effect was especially remarkable in the soleus, which is particularly sensitive to oxidative stress, as revealed by the increased vitamin E level and SOD and GPx activities.

Exercise-induced attenuation of obesity, hyperinsulinemia, and skeletal muscle lipid peroxidation in the OLETF rat

The Otsuka Long-Evans Tokushima fatty (OLETF) rat is a model of hyperphagic obesity in which the animals retain the desire to run voluntarily. Running wheels were provided for 4-wk-old OLETF rats for 16 wk before they were killed 5 h (WL5), 53 h (WL53), or 173 h (WL173) after the wheels were locked. Sedentary (SED) OLETF rats that were not given access to running wheels served as age-matched cohorts. Epididymal fat pad mass, adipocyte volume, and adipocyte number were 58%, 39%, and 47% less, respectively, in WL5 than SED rats. Contrary to cessation of daily running in Fischer 344 x Brown Norway rats, epididymal fat did not increase during the first 173 h of running cessation in the OLETF runners. Serum insulin and glucose levels were 77% and 29% less, respectively, in WL5 than SED rats. Oil red O staining for intramyocellular lipid accumulation was not statistically different among groups. However, lipid peroxidation levels, as determined by total trans-4-hydroxy-2-nonenal (4-HNE) and 4-HNE normalized to oil red O, was higher in epitrochlearis muscles of SED than WL5, WL53, and WL173 rats. mRNA levels of glutathione S-transferase-alpha type 4, an enzyme involved in cellular defense against electrophilic compounds such as 4-HNE, were higher in epitrochlearis muscle of WL53 than WL173 and SED rats. In contrast, 4-HNE levels in omental fat were unaltered. Epitrochlearis muscle palmitate oxidation and relative transcript levels for peroxisome proliferator-activated receptor-delta and peroxisome proliferator-activated receptor-gamma coactivator type 1 were surprisingly not different between runners and SED rats. In summary, voluntary running was associated with lower levels of lipid peroxidation in skeletal muscle without significant changes in intramyocellular lipids or mitochondrial markers in OLETF rats at 20 wk of age. Therefore, even in a genetic animal model of extreme overeating, daily physical activity promotes improved health of skeletal muscle.

Effects of increased dietary fat and exercise on skeletal muscle lipid peroxidation and antioxidant capacity in male rats

Elevated dietary fat increases oxidative metabolism and has been linked to increased oxidative stress, while exercise training may augment antioxidant capacity. Most studies examining oxidative stress in skeletal muscle employ extremely high levels of dietary fat and/or intense exercise training that may not adequately model human diet and activity patterns. The purpose of this study was to examine the interaction between an elevated (40% of calories) monounsaturated fat diet and a moderate-intensity exercise program similar to recommended human exercise prescriptions, on skeletal muscle oxidative stress and antioxidant defenses. Twenty-four male Sprague-Dawley rats (approximately 500 g) were randomly divided into 4 groups (n = 6/group): Standard Diet-Sedentary (SD-Sed), Standard Diet-Exercise (SD-Ex), Elevated Fat Diet-Sedentary (EFD-Sed), and Elevated Fat Diet-Exercise (EFD-Ex). The SD groups consumed 76% of calories from CHO, 14% from protein, and 10 % from fat, while the EFD groups received a diet of 46% of calories from CHO, 14% from protein, and 40 % from fat (high oleic sunflower oil). The exercise groups were progressively treadmill trained at 20 m/min, 4 days/week increasing from 15 min/day to 35 min/day by the end of 4 wks. Antioxidant adaptations associated with exercise training or an elevated fat diet individually reduced basal lipid peroxidation levels in the plantaris muscle. However, the combination of exercise plus a monounsaturated fat diet increased lipid peroxidation levels above that with either treatment alone. This suggests an exhaustion of the antioxidant capacity in the plantaris muscle when both exercise and increased dietary fat diet are combined.

Lipid peroxidation in skeletal muscle of obese as compared to endurance-trained humans: a case of good vs. bad lipids?

Intra-myocellular triglycerides (IMTG) accumulate in the muscle of obese and endurance-trained (ET) humans and are considered a pathogenic factor in the development of insulin resistance, in the former. We postulate that this paradox may be associated with the peroxidation status of the IMTG. IMTG content was the same in the obese and ET subjects. The lipid peroxidation/IMTG ratio was 4.2-fold higher in the obese subjects. Hence, obesity results in an increased level of IMTG peroxidation while ET has a protective effect on IMTG peroxidation. This suggests a link between the lipid peroxidation/IMTG ratio and insulin resistance.

Influence of diagnostic categories, age, and gender on antioxidative defense and lipid peroxidation in skeletal muscle of patients with neuromuscular diseases

The influence of diagnostic categories, age, and gender on parameters of oxidative stress measured in 102 patients with neuromuscular diseases and 11 control subjects was assessed using a stepwise multiple linear regression model. Antioxidative enzyme activities, lipophilic antioxidants, and lipid peroxidation were analyzed in muscle biopsies. Mitochondrial myopathies and amyotrophic lateral sclerosis (ALS) are thought to be particularly susceptible to increased oxidative stress. In our study, mitochondrial myopathies emerged as a positive predictor of malondialdehyde (p < 0.05) and ALS as a negative predictor of alpha-tocopherol (p < 0.05). Although the primary atrophic process in ALS is not in muscle but in motoneurons, this finding could have therapeutic implications, as such patients might benefit from antioxidant supplementation. In our study age emerged as a negative predictor of the coenzyme Q10 concentration (p < 0.003), whereas the percentage of reduced coenzyme Q10 remained unchanged. Age emerged as a positive predictor of the activities of catalase (p < 0.01) and superoxide dismutase (p < 0.002), probably reflecting an enzymatic upregulation that compensates for the loss of coenzyme Q10. The increased activities of catalase and superoxide dismutase in females compared to males indicate a higher antioxidative potential in female muscle. Whether this increase contributes to a higher life expectancy of women remains to be investigated.

High Altitude Training Increases Reactive Carbonyl Derivatives But Not Lipid Peroxidation in Skeletal Muscle of Rats

The oxidative stress related consequences of physical training at high altitude are not known. The hypothesis was tested that physical training and exposure to high altitude have adverse effects on free radical generation and activities of antioxidant enzymes. The present results showed that 4 weeks of exercise at an altitude of 4000 m increased the activity of Mn-SOD in both white and red types of skeletal muscle. The activities of Cu,Zn-SOD, catalase, and glutathione peroxidase, as well as the level of lipid peroxidation measured by TBARS and lipid hydroperoxides, did not change significantly. In contrast, the level of reactive carbonyl derivatives measured by anti-2,4-dinitrophenylhydrazone antibodies and spectrophotometry showed an increase in both types of muscle of altitude trained rats compared with sea level trained and control groups. It was suggested that the oxidative modification of certain amino acids is due to the increasing gap between activity of SOD and peroxide scavenging enzymes, which results in increases in the number of hydrogen peroxide molecules. Thus, since the mechanism of generation and/or the mode of action of radicals resulting in lipid peroxidation and protein oxidation appears to be different in vivo, both processes should be studied during oxidative stress. Copyright © 1997 Elsevier Science Inc.

Deferoxamine prevents lipid peroxidation and attenuates reoxygenation injury in postischemic skeletal muscle

In the presence of the transition metal iron, superoxide anion and H2O2 generated on reperfusion of postichemic tissue combine to form hydroxyl radical, which readily attacks membrane-associated polyunsaturated fatty acids in a free radical process, resulting in lipid peroxidation. To evaluate whether iron chelation with deferoxamine interrupts this process in postischemic skeletal muscle, high-grade partial hindlimb ischemia was created in Sprague-Dawley rats by clamping the infrarenal aorta for 90 min, after which period the clamp was removed and flow was reestablished for 60 min. Lipid peroxidation in skeletal muscle was assessed by determination of tissue thiobarbituric acid-reactive substances (TBARS); membrane dysfunction was assessed by measurement of resting membrane potential (Em). Ischemia was accompanied by an increase in muscle TBARS and depolarization of resting Em. On reperfusion, muscle TBARS continued to increase, whereas resting Em remained depolarized. Pretreatment with deferoxamine prevented lipid peroxidation during ischemia but had no effect on resting Em. On reperfusion in the deferoxamine-treated animals, there was still no increase in muscle TBARS, and partial repolarization of resting Em was noted. It is concluded that 1) high-grade partial ischemia in skeletal muscle is accompanied by iron-dependent lipid peroxidation via a mechanism that persists and accelerates on reoxygenation, 2) lipid peroxidation impacts on functional membrane integrity during the reperfusion phase only, and 3) membrane injury accompanying ischemia and reperfusion may occur through fundamentally different mechanisms, of which only the latter is iron dependent.