Antioxidant Defense Markers Research Articles

Effect of Moderate and High Resistance Training Intensity on Indices of Inflammatory and Oxidative Stress

This study was designed to examine the effect of moderate (MR) and high resistance (HR) training on systemic inflammation and circulating enzymatic antioxidant activity. Thirty males were assigned to HR (n = 10), MR (n = 10), or control (C; n = 10) groups. Resistance training was performed for eight weeks. Activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), creatine kinase (CK), and concentrations of malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured before and after training in plasma. The results show increased SOD activity in MR (p = 0.026) and HR (p = 0.044) groups. GPX activity in HR (p = 0.012) and MR (p = 0.037) increased significantly more than in C. Whilst a significant reduction in MDA in MR (p = 0.013) and HR (p = 0.023) was observed compared with C, no significant difference in IL-6, TNF-α and CK occurred between groups. We conclude that changes in enzymatic antioxidant defense and inflammatory markers following resistance training are independent of training intensity.

Effects of grape seed extract on oxidative stress and antioxidant defense markers in streptozotocin-induced diabetic rats.

To evaluate the effects of grape seed extract (GSE) supplementation on oxidative stress and antioxidant markers in streptozotocin (STZ)-induced diabetic rats. Thirty-six male rats were divided into the following four groups: control, GSE-supplemented control, diabetic, and GSE-supplemented diabetic. Beginning on day 7 after STZ injection, the rats were administered GSE (100 mg kg(-1) day(-1) in drinking water for 6 weeks. At the end of week 6, rats were sacrificed by cardiac puncture. Plasma nitric oxide (NO) levels and xanthine oxidase (XO), adenosine deaminase (ADA), and glutathione peroxidase (GPx) activities were analyzed. Both XO and ADA activities increased and NO levels decreased in diabetic rats (P < 0.05). GSE supplementation normalized all of these changes. Antioxidant enzyme activities decreased in diabetic rats compared to the controls (P < 0.05). GSE supplementation increased antioxidant enzyme activities in both diabetic and healthy rats (P < 0.05). These findings suggest that 6 weeks of oral GSE supplementation may prevent oxidative stress and improve antioxidant status in diabetic rats.

Influence of Different Doses of Levofloxacin on Antioxidant Defense Systems and Markers of Renal and Hepatic Dysfunctions in Rats

Levofloxacin (LFX) is a broad spectrum fluoroquinolone antibiotic used in the treatment of infections such as pneumonia, chronic bronchitis, and sinusitis. The present study assessed the likely toxic effect of LFX on hepatic and renal tissues in rats. Twenty male Wistar rats were randomly divided into four treatment groups: A: control, B: 5 mg/kg bw LFX (half therapeutic dose), C: 10 mg/kg bw LFX (therapeutic dose), and D: 20 mg/kg bw LFX (double therapeutic dose). After seven days of administration, result indicated significant(P&lt;0.05)increase in plasma ALT, AST, and ALP activities in the treated groups compared to control. Also, there was a significant increase in plasma creatinine, urea, and total bilirubin in the treated groups relative to control. Plasma total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglycerides also increased significantly in the treated groups relative to control. Also, hepatic MDA level increased significantly in all the treated groups. However, hepatic SOD, catalase, and GST activities were significantly reduced in the LFX-treated animals. Moreover, GSH and ascorbic acid levels were significantly decreased in the LFX-treated groups relative to control. In conclusion, three doses of levofloxacin depleted antioxidant defense system and induced oxidative stress and hepatic and renal dysfunctions in rats.

Salivary glucose and antioxidant defense markers in type II diabetes mellitus.

To evaluate salivary antioxidant defense markers, their correlation with salivary glucose, and glycemic status in type II diabetes mellitus (DM). The study included 53 diabetic patients and 40 healthy subjects. Salivary glucose, blood glucose, and uric acid (UA) were determined by specific enzymatic methods. Total antioxidant activity (AOA), glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and total protein were determined spectrophotometrically. Salivary UA (3.12 vs. 1.89 mg/dL), GSH (47 vs. 11.92 jg/mL), and total protein (375.12 vs. 202.23 mg/dL) were significantly higher (P < 0.001; r = 0.455, 0.735, 0.498 respectively) and AOA (653.1 vs. 897.3 µmol/L) was significantly lower in the DM group (P <0.001, r = -0.431) compared to healthy controls. Among the antioxidant enzymes, CAT was significantly lower (1214 vs. 9468.9 kat) in the DM group (P < 0.001, r = -0.886). Spearman correlation analyses within the diabetic group showed a strong positive association between salivary glucose and blood glucose (P <0.001, r = 0.9), salivary glucose and GSH, and salivary glucose and UA. Salivary glucose showed a negative correlation with AOA and CAT (P = 0.008, r = -0.447) in the diabetic group. Findings of this study, showing a strong correlation between salivary glucose and blood glucose as well as changes in antioxidant components in the DM group, suggest that saliva can be used for the diagnosis and management of DM.

Peripheral markers of oxidative stress and antioxidative defense in euthymia of bipolar disorder—Gender and obesity effects

IntroductionOxidative and nitrosative stress are implicated in the pathogenesis of uni- and bipolar disorder. Herein we primarily sought to characterize markers of oxidative/nitrosative stress during euthymia in adults with bipolar disorder (BD). Oxidative markers were further evaluated in this BD sample in synopsis with excess overweight or obesity and/or comorbid metabolic syndrome (MetS). MethodsPeripheral markers of oxidative stress [i.e. thiobarbituric acid reactive substance, (TBARS), malondialdehyde (MDA), and carbonyl proteins] and antioxidant markers [e.g. total antioxidative capacity (TAC), superoxide dismutase (SOD), glutathione S-transferase (GST)] were obtained in a cohort of euthymic adults with BD (N=113) and compared to healthy controls (CG) (N=78). Additionally, anthropometric measures included the body mass index (BMI) [kg/m2], waist and hip circumference [cm], waist-to-hip-ratio (WHR), waist to height ratio (WtHR) as well as the IDF-defined MetS. ResultsThe major finding was a significantly decreased TAC in BD compared to the CG (p<0.01; BD: M 1.18, SD 0.47; CG: M 1.39, SD 0.49). MDA was significantly and TBARS by trend higher in the CG compared to the euthymic bipolar test persons (MDA: p<0.01, BD: M 0.70, SD 0.18; CG: M 0.81, SD 0.25; TBARS: p<0.1, BD: M 0.78, SD 0.28; CG: M 0.76, SD 0.30). The antioxidative enzyme GST was significantly elevated in both patients and controls (BD: M 298.24, SD 133.02; CG: M 307.27 SD 118.18). Subgroup analysis revealed that the CG with concurrent MetS and obesity had significantly elevated TAC when compared to CG without concurrent MetS (p<0.05, no MetS: M 1.33, SD 0.50; MetS: M 1.67, SD 0.32), as well as persons with BD with or without current MetS (no MetS: M 1.18, SD 0.44; MetS: M 1.15, SD 0.49). Significant correlations between GST and anthropometric variables were found in male study participants. Multivariate analysis indicated a significant gender effect concerning TBARS values in all patients and CG (p<0.01, females: M 0.73, SD 0.29; males: M 0.83, SD 0.28). ConclusionEuthymic bipolar adults exhibit peripheral evidence of a disturbed biosignature of oxidative stress and antioxidative defense. Male test persons showed significantly higher peripheral markers of oxidative stress than women- female sex may exert protective effects. Furthermore, the biosignature of oxidative stress obtained herein was more pronounced in males with concurrent metabolic disorders. Our results further extend knowledge by introducing the moderating influence of gender and obesity on oxidative stress and BD.

Metabolic and transcriptional responses of gilthead sea bream (Sparus aurata L.) to environmental stress: New insights in fish mitochondrial phenotyping

The aim of the current study was to phenotype fish metabolism and the transcriptionally-mediated response of hepatic mitochondria of gilthead sea bream to intermittent and repetitive environmental stressors: (i) changes in water temperature (T-ST), (ii) changes in water level and chasing (C-ST) and (iii) multiple sensory perception stressors (M-ST). Gene expression profiling was done using a quantitative PCR array of 60 mitochondria-related genes, selected as markers of transcriptional regulation, oxidative metabolism, respiration uncoupling, antioxidant defense, protein import/folding/assembly, and mitochondrial dynamics and apoptosis. The mitochondrial phenotype mirrored changes in fish performance, haematology and lactate production. T-ST especially up-regulated transcriptional factors (PGC1α, NRF1, NRF2), rate limiting enzymes of fatty acid β-oxidation (CPT1A) and tricarboxylic acid cycle (CS), membrane translocases (Tim/TOM complex) and molecular chaperones (mtHsp10, mtHsp60, mtHsp70) to improve the oxidative capacity in a milieu of a reduced feed intake and impaired haematology. The lack of mitochondrial response, increased production of lactate and negligible effects on growth performance in C-ST fish were mostly considered as a switch from aerobic to anaerobic metabolism. A strong down-regulation of PGC1α, NRF1, NRF2, CPT1A, CS and markers of mitochondrial dynamics and apoptosis (BAX, BCLX, MFN2, MIRO2) occurred in M-ST fish in association with the greatest circulating cortisol concentration and a reduced lactate production and feed efficiency, which represents a metabolic condition with the highest allostatic load score. These findings evidence a high mitochondrial plasticity against stress stimuli, providing new insights to define the threshold level of stress condition in fish.

Effects of Polyphenol-Rich Chokeberry Juice on Antioxidant/Pro-Oxidant Status in Healthy Subjects

Berry fruits are a rich source of polyphenols, especially anthocyanins: well-known potent anti-oxidant phytochemicals. The purpose of this study was to evaluate beneficial effects of long-term consumption of polyphenol-rich organic chokeberry juice on different markers of antioxidant/pro-oxidant status in healthy female volunteers. Twenty-nine women, aged 25-49, were included in the study. Serological markers of oxidative stress and antioxidant defence, blood pressure, routine biochemical, and anthropometric parameters were analyzed at baseline and after twelve weeks of regular chokeberry juice consumption. Significant decrease in thiobarbituric acid-reactive substances level (TBARS; P<.001) and pro-oxidant-antioxidant balance (PAB; P<.05), as well as increase in paroxonase-1 activity toward diazoxon (P<.01) were found. Total oxidative status and sulphydryl groups levels were not significantly influenced by the intervention. Anthropometric, biochemical parameters, and blood pressure values were within the referent values for all subjects and were not influenced by the chokeberry juice consumption. However, we found positive correlation between age, body mass index, waist circumference, body fat percent, blood pressure, and analyzed marker of lipid peroxidation, which was influenced by the consumption. In conclusion, the fine modulation of several antioxidant/pro-oxidant status biomarkers observed in healthy subjects indicates putative prophylactic effects of polyphenol-rich chokeberry juice and supports its importance as part of an optimal diet.

Exogenous Nitric Oxide (as Sodium Nitroprusside) Ameliorates Polyethylene Glycol-Induced Osmotic Stress in Hydroponically Grown Maize Roots

The present study was designed to examine whether exogenous sodium nitroprusside (SNP) supplementation has any ameliorating action against PEG-induced osmotic stress in Zea mays cv. FRB-73 roots. Twenty percent or 40 % polyethylene glycol (PEG6000; −0.5 MPa and −1.76 MPa, respectively) treatment alone or in combination with 150 and 300 μM SNP was applied to hydroponically grown maize roots for 72 h. Although only catalase (CAT) activity increased when maize roots were exposed to PEG-induced osmotic stress, induction of this antioxidant enzyme was inadequate to detoxify the extreme levels of reactive oxygen species, as evidenced by growth, water content, superoxide anion radical (O 2 •− ), hydroxyl radical (OH•) scavenging activity, and TBARS content. However, supplementation of PEG-exposed specimens with SNP significantly alleviated stress-induced damage through effective water management and enhancement of antioxidant defense markers including the enzymatic/non-enzymatic systems. Exogenously applied SNP under stress resulted in the up-regulation of glutathione peroxidase (GPX), glutathione S-transferase (GST), ascorbate peroxidase (APX), glutathione reductase (GR), total ascorbate, and glutathione contents involved in ascorbate–glutathione cycle. On the other hand, growth rate, osmotic potential, CAT, APX, GR, and GPX increased in maize roots exposed to both concentrations of SNP alone, but activities of monodehydroascorbate reductase (MDHAR) and dehydroascorbate reductase decreased. Based on the above results, an exogenous supply of both 150 and 300 μM SNP to maize roots was protective for PEG-induced toxicity. The present study provides new insights into the mechanisms of SNP (NO donor) amelioration of PEG-induced osmotic stress damages in hydroponically grown maize roots.

Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review.

Normal aging involves a gradual breakdown of physiological processes that leads to a decline in cognitive functions and brain integrity, yet the onset and progression of decline are variable among older individuals. While many biological changes may contribute to this degree of variability, oxidative stress is a key mechanism of the aging process that can cause direct damage to cellular architecture within the brain. Oligodendrocytes are at a high risk for oxidative damage due to their role in myelin maintenance and production and limited repair mechanisms, suggesting that white matter may be particularly vulnerable to oxidative activity. Antioxidant defense enzymes within the brain, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), are crucial for breaking down the harmful end products of oxidative phosphorylation. Previous studies have revealed that allele variations of polymorphisms that encode these antioxidants are associated with abnormalities in SOD, CAT, GPx, and GST activity in the central nervous system. This review will focus on the role of oxidative stress in the aging brain and the impact of decreased antioxidant defense on brain integrity and cognitive function. Directions for future research investigations of antioxidant defense genes will also be discussed.

Effects of Chow and Liquid Diet on Liver Integrity and Antioxidant Defense in Sleep-Deprived Male Rats

The influence of diet composition and availability on liver and antioxidant system function under sleep deprivation (SD) in rats is not completely known. We have previously demonstrated that chow-fed sleep-deprived rats lose weight and present a starvation-like metabolic and hormonal profile, accompanied by hyperphagia. On the other hand, liquid diet attenuates weight loss and the endocrine-metabolic effects associated to SD. It is widely known that energy metabolism is strongly correlated with the production of free radicals and that oxidative cell damage may occur. Our objective was to verify whether the two different diets offered during SD would also affect antioxidant defense system and liver integrity. Male rats were distributed into the following groups: control, sleep-deprived for 96 h by the platform technique (SD-96h) or SD-96h recovered for 24 h (Rebound). Rats were fed with chow pellets (CP) or a liquid diet (LD). Our results show that the CP rats showed changes in antioxidant defense parameters and liver damage markers after SD. However, such changes were attenuated in rats fed the liquid diet. We conclude that the attenuated effect of LD on some studied liver damage and antioxidant defense markers lead us to suggest that these changes are at least partially linked to energy deficits induced by SD.

Changes in physiological responses of an Antarctic fish, the emerald rock cod (Trematomus bernacchii), following exposure to polybrominated diphenyl ethers (PBDEs)

Although polybrominated diphenyl ethers (PBDEs) have the ability to undergo long-range atmospheric transport to remote ecosystems like Antarctica, a recent study found evidence for a local source within the Antarctic. PBDEs from sewage treatment outfalls of McMurdo Station and Scott Base on Ross Island have been attributed to the high concentrations measured in emerald rock cod (Trematomus bernacchii). The potential impact of PBDEs on Antarctic fish physiology is unknown and therefore, the aim of this study was to obtain a greater understanding of physiological responses of emerald rock cod for assessing changes in ecosystem quality. A PBDE mixture (ΣPBDE 8 congeners) was administered fortnightly over 42 days and physiological changes were observed throughout this period and for a further 14 days thereafter. Changes in liver composition, molecular level changes and enzyme activities of selected detoxification-mediated and antioxidant defence markers were measured. Changes in total lipid, lipid peroxide and protein carbonyl concentrations in emerald rock cod liver were consistent with increases in nucleus surface area in the PBDE-treated groups, suggesting alterations in cellular function. Changes in the activities of selected antioxidant enzymes indirectly indicated oxidative stress, possibly resulting in the changes in liver composition. Additionally, glutathione-S-transferase (GST) activity reached its peak faster than that of ethoxyresorufin-O-deethylase (EROD), suggesting that during the early response to PBDE exposures there could be a greater involvement of GST-mediated detoxification. Thus, for at least the species examined here, protein carbonyl and lipid peroxides were useful and informative biomarkers for cellular level responses following PBDE-related exposure. Furthermore, our findings suggest that emerald rock cod exposed to PBDEs develop oxidative stress – a condition with potential consequences for fish growth, health and reproduction.

Influence of coadministration of artemether and lumefantrine on selected plasma biochemical and erythrocyte oxidative stress indices in female Wistar rats

Among the artemisinin-based combination therapy (ACT) regimens, artemisinin derivative, artemether in combination with lumefantrine (artemether-lumefantrine, AL) has achieved excellent results in the fight against malarial scourge. In this study, we evaluated the toxic potential of these drugs at the therapeutic doses in female Wistar rats. Animals were randomly divided into four groups: those administered 1% Tween 80 (control), those administered artemether (4mg/kg body weight), those administered lumefantrine (24mg/kg body weight), and those coadministered artemether (4mg/kg body weight) and lumefantrine (24mg/kg body weight). The drugs were orally administered twice daily for 3 days by gastric intubation after which selected plasma biochemical indices, and erythrocytes antioxidant defence and lipid peroxidation markers were evaluated. Coadministration of artemether and lumefantrine raised liver and renal function markers and increased atherogenic index. While reduced glutathione, glucose-6-phosphate dehydrogenase (G6PD) and catalase activities were reduced, glutathione peroxidase and glutathione-s-transferase activities increased in all the treated groups compared to the control group. The drugs caused significant (p<0.05) elevation of malondialdehyde (MDA) levels compared to the control group. These results imply that coadministration of artemether and lumefantrine may increase the risks of atherosclerosis as well as liver and renal function impairments in the users. In addition, the drugs may also promote oxidative stress in the erythrocytes.

Bolus Consumption of a Specifically Designed Fruit Juice Rich in Anthocyanins and Ascorbic Acid Did Not Influence Markers of Antioxidative Defense in Healthy Humans

Exotic fruits such as açai, camu-camu, and blackberries rich in natural antioxidants (ascorbic acid, anthocyanins) are marketed as "functional" foods supporting a pro-/antioxidant balance. Confirming data from human studies are lacking. Within a randomized controlled crossover trial, 12 healthy nonsmokers ingested 400 mL of a blended juice of these fruits or a sugar solution (control). Blood was drawn before and afterward to determine antioxidants in plasma, markers of antioxidant capacity [trolox equivalent antioxidant capacity, Folin-Ciocalteu reducing capacity, total oxidant scavenging capacity (TOSC)] and oxidative stress [isoprostane, DNA strand breaks in leukocytes in vivo], and their resistance versus H₂O₂-induced strand breaks. Compared with sugar solution, juice consumption increased plasma ascorbic acid and maintained TOSC and partly Folin-Ciocalteu reducing capacity (both P values < 0.05). Strand breaks in vivo increased after ingestion of both beverages (P < 0.001), probably due to postprandial and/or circadian effects. This anthocyanin-rich fruit juice may stabilize the pro-/antioxidant balance in healthy nonsmokers without affecting markers of oxidative stress.

Effects of Grape Seed Polyphenols on Oxidative Damage in Liver Tissue of Acutely and Chronically Exercised Rats

The objective of the present study was to investigate the effects of grape seed extract (GSE) supplementation on oxidative stress and antioxidant defense markers in liver tissue of acutely and chronically exercised rats. Rats were randomly assigned to six groups: Control (C), Control Chronic Exercise (CE), Control Acute Exercise (AE), GSE-supplemented Control (GC), GSE-supplemented Chronic Exercise(GCE) and GSE-supplemented Acute Exercise (GAE). Rats in the chronic exercise groups were subjected to a six-week treadmill running and in the acute exercise groups performed an exhaustive running. Rats in the GSE supplemented groups received GSE (100 mg.kg(-1) .day(-1) ) in drinking water for 6 weeks. Liver tissues of the rats were taken for the analysis of malondialdehyde (MDA), nitric oxide (NO) levels and total antioxidant activity (AOA) and xanthine oxidase (XO) activities. MDA levels decreased with GSE supplementation in control groups but increased in acute and chronic exercise groups compared to their non-supplemented control. NO levels increased with GSE supplementation. XO activities were higher in AE group compared to the CE group. AOA decreased with GSE supplementation. In conclusion, while acute exercise triggers oxidative stress, chronic exercise has protective role against oxidative stress. GSE has a limited antioxidant effect on exercise-induced oxidative stress in liver tissue.

High-fat diet feeding induces a depot-dependent response on the pro-inflammatory state and mitochondrial function of gonadal white adipose tissue

Obesity has been related to a chronic pro-inflammatory state affecting white adipose tissue (WAT), which has a great impact on carbohydrate, lipid and energy metabolism. In turn, the dysregulation of adipokine secretion derived from the accumulation of excess lipids in adipocytes further contributes to the development of insulin resistance and can be associated with mitochondrial dysfunction. The aim of the present study was to determine whether sexual dimorphism found in the systemic insulin sensitivity profile is related to sex differences in a high-fat diet (HFD) response of gonadal WAT at mitochondrial function and inflammatory profile levels. Wistar rats (10 weeks old) of both sexes were fed a control pelleted diet (3 % (w/w) fat; n 8 for each sex) or a HFD (24 % (w/w) fat; n 8 for each sex). Serum insulin sensitivity markers, mRNA expression levels of inflammatory factors and the protein content of insulin and adiponectin signalling pathways were analysed, as well as the levels of the main markers of mitochondrial biogenesis, antioxidant defence and oxidative damage. In the present study, the periovarian depot exhibits a greater expandability capacity, along with a lower hypoxic and pro-inflammatory state, without signs of mitochondrial dysfunction or changes in its dynamics. In contrast, epididymal fat has a much more pronounced pro-inflammatory, hypoxic and insulin-resistant profile accompanied by changes in mitochondrial dynamics, probably associated with HFD-induced mitochondrial dysfunction. Thus, this explains the worse serum insulin sensitivity profile of male rats.

Redox balance and mitochondrial glycerol phosphate dehydrogenase activity in trained rats

Free radical production is increased in many disease states and during exercise, but in the latter the concurrent stimulation of the antioxidant defense system seems to protect the organism from excessive production of reactive oxygen species. Chronic exercise can exert negative effects on the activity of mitochondrial glycerol phosphate dehydrogenase (mGPdH), which may offer some explanation for the antioxidant effects of training, since this enzyme is a relevant producer of free radicals. To test this correlation, we compared mGPdH activity, two antioxidant defense markers and two markers of oxidative stress in sedentary and trained (Tr) rats. Training was through a swimming exercise 3days a week. After 8weeks, Tr rats lasted twice as long as controls in an acute swimming test with a 5% load. Forty-eight hours after the last exercise, the animals were killed to collect blood and tissues. Tr animals presented lower body weight and visceral fat mass with lower triglyceride content in visceral fat and plasma (p<0.05). The specific activity of mGPdH in muscle mitochondria was reduced in Tr rats by 88% (p<0.05). Total antioxidant capacity, lipid peroxidation and reduced glutathione (GSH) in liver and muscle were unaltered, while plasma GSH increased by 21% (p<0.05). These data suggest a profile of successful redox equilibrium maintenance in Tr rats, with a potentially significant contribution from the lower level of mGPdH activity in muscle. This training protocol appears to be suitable for use in detailed studies of biochemical adaptations to oxidative stress.

Quercetin protects against testicular toxicity induced by chronic administration of therapeutic dose of quinine sulfate in rats

Quinine, a rapidly acting blood schizonticide with a long history of use for the treatment of malaria, is gradually been implicated in reproductive toxicity. In this study, testicular and spermatotoxic effects of quinine sulfate (QS) following treatment with an oral dose of 10 mg/kg/day (normal therapeutic dose) for 8 weeks was investigated in male albino rats. Toxicity was evaluated by assessing antioxidant defense capacity and markers of oxidative stress and testicular dysfunction in the testes and epididymal sperm. The possible ameliorative effect of quercetin (QC), when co-administered with QS, was also assessed. Administration of QS induced oxidative stress in rats. The activities of superoxide dismutase, catalase, and malondialdehyde (a marker of lipid peroxidation) increased (p<0.05) both in the testes and epididymal sperm following QS treatment when compared with saline-treated (control) rats. Ascorbic acid levels were significantly reduced, with an insignificant decrease in glutathione and testosterone levels in the QS-treated rats, when compared with control. The spermiogram decreased with increase in total sperm abnormalities in QS-treated rats and was associated with histopathological changes. Our results revealed that QC significantly ameliorated QS-induced testicular toxicity and oxidative stress. The testicular toxicity of QS is in part due to impairment of testicular antioxidant defense, spermatogenesis and enhancement of lipid peroxidation. Also, the ability of QC to reverse the deleterious effects of QS on the testes and epididymis qualifies it as a potent chemo-protective agent against QS-induced reproductive toxicity.

Influence of Punica granatum L. on region specific responses in rat brain during Alloxan-Induced diabetes

ObjectiveThe present study was carried out to investigate the effects of Punica granatum peel methanolic extract (PGPE) on cerebral cortex (CC) and Hippocampus (HC) brain antioxidant defense system and markers of lipid and protein oxidation in alloxan induced diabetic rats. MethodsOral administration of PGPE (75 and 150 mg of kg body weight) for 45 days resulted in significant reduction in blood glucose levels. ResultsSupplementation of diabetic rats with PGPE showed increased activities of SOD and GPx with concomitant decrease in MDA and PC content. Region-specific changes were more evident in the HC when compared to CC. ConclusionsThe present study indicated that PGPE can ameliorate brain oxidative stress in alloxan induced diabetic rats by up regulating antioxidant defense mechanism by attenuating lipid and protein oxidation. PGPE thus may be used as a potential therapeutic agent in preventing diabetic complications in the brain.

Effects of ovariectomy and 17-β estradiol replacement on rat brown adipose tissue mitochondrial function

Taking into account the sexual dimorphism previously reported regarding mitochondrial function and biogenesis in brown adipose tissue, the aim of the present study was to go further into these differences by investigating the effect of ovariectomy and 17-β estradiol (E2) replacement on brown adipose tissue mitochondrial function. In this study, fourteen-week-old control female and ovariectomized female Wistar rats were used. Rats were ovariectomized at 5 weeks of age and were treated every 2 days with placebo (OVX group) or E2 (10 μg/kg) (OVX + E2 group) for 4 weeks before sacrifice. We studied the levels of oxidative capacity, antioxidant defence and oxidative damage markers in brown adipose tissue. Moreover, the levels of key elements of mitochondrial biogenesis as well as UCP1 protein levels, as an index of mitochondrial thermogenic capacity, were also determined. In response to ovariectomy, mitochondrial proliferation increased, resulting in less functional mitochondria, since oxidative capacity and antioxidant defences decreased. Although E2 supplementation was able to restore the serum levels of E2 shown by control rats, the treatment reverted the effects of the ovariectomy only in part, and oxidative and antioxidant capacities in OVX + E2 rats did not reach the levels shown by control females. Taking these results into account, we suggest that ovarian hormones are responsible, at least in part, for the sexual dimorphism in BAT mitochondrial function. However, other signals produced by ovary, rather than E2, would play an important role in the control of mitochondrial function in BAT.

Correlation of Oxidative Stress Parameters and Inflammatory Markers in Tunisian Coronary Artery Disease Patients

Introduction: Oxidative stress is now recognized as being the cause and the consequence of cardiovascular diseases. Objective: The role that oxidative stress parameters and inflammatory markers may play in diabetes and related cardiovascular disease (CVD) among Tunisian coronary diabetic patients. Patients and methods: We measured the erythrocyte glutathione peroxidase (GPX), the superoxide dismutase (SOD) activities and the plasmatic total antioxidant status (TAS) concentration by colorimetric methods, the hs-CRP by immunonephelometry assays. Results: TAS and GPX were significantly decreased among patients compared to the controls (1.14 ± 0.28 mmol/l vs 1.55 ± 0.35 mmol/l; 59.32 ± 10.72 U/gHb vs 149.19 ± 30.95 U/gHb). For the diabetic patients, TAS is correlated positively with hs-CRP (r=0.01, p&lt;10-3). At the not diabetic subjects, TAS is correlated negatively with the hsCRP. Conclusion: Determination of antioxidative defense markers contributes to understanding the effect of stress oxidative on the development and the prevention of cardiovascular disease.