Betaine Elevates Ovarian Antioxidant Enzyme Activities and Demonstrates Methyl Donor Effect in Non-Pregnant Rats

Chronic alcoholism leads to infertility in male and female rats, and antioxidant enzymes form the first line against oxidative stress in organisms. In recent years, betaine has shown beneficial effects on various tissues, and this study has attempted to clarify antioxidant and methyl donor properties of betaine in the rat ovary. For this purpose, the sexually matured Sprague-Dawley female rats were divided into Control, Ethanol (EtOH), Betaine, and Betaine?+?EtOH groups. Administration of betaine in Betaine?+?EtOH group significantly increased CAT activity when compared to the other groups (P?<?0.05). GPx activity increased significantly in Betaine and Betaine?+?EtOH groups as compared to controls (P?<?0.05). Interestingly, GPx and CAT activities insignificantly increased (in order compensatory) in EtOH group to suppress oxidative stress. In contrast, SOD activity decreased insignificantly in EtOH group compared to Betaine?+?EtOH and control groups (P?>?0.05). TBARS concentration (as a lipid peroxidation marker) significantly increased in ethanol-treated rats as compared to controls, while total homocysteine concentration significantly decreased in betaine-treated rats in comparison with EtOH group. Regarding to oestrous cycles, ethanol-treated animals had irregular estral cycle and persistent oestrous phase compared to controls and betaine-treated rats. In conclusion, these results demonstrate for the first time the antioxidant and methyl donor properties of betaine in the rat ovary. Thus, betaine might be used as a potential therapy in hyperhomocysteinemia and partial infertility mediated by oxidative stress in females.     

Chlorpyrifos Induced Region Specific Vulnerability in Rat CNS and Modulation by Age and Cold Stress: An Interactive Study

Chlorpyrifos (CPF), an organophosphorus insecticide is known to cause ill health in non-target animals by inducing oxidative stress. In this study influence of cold stress (15°C and 20°C) and age as modulating factors on CPF induced oxidative stress was addressed to assess age-related differences and vulnerability in central nervous system of rats. The results indicated an interaction with age and cold exposure resulting in marked decreased activity levels of SOD (P < 0.05), CAT (P < 0.05), GPx (P < 0.05), GST (P < 0.05) followed by increased MDA (P < 0.05) and decreased GSH levels (P < 0.05). The ANOVA and Post-hoc analysis showed that antioxidant enzymes decreased significantly (P < 0.05) on CPF exposure. Moreover synergistic action of CPF and cold stress at 15°C caused higher inhibition on comparison with CPF and cold stress alone and together at 20°C indicating the extent of peroxidative damage in discrete regions of CNS. Further this study showed young individuals to be more sensitive than adults.     

Antioxidant status in patients with psoriasis

Psoriasis is a chronic inflammatory skin disease with an unknown aetiology that has been associated with abnormal plasma lipid metabolism and oxidative stress. There are controversial results in the previous studies investigating oxidant/antioxidant systems in psoriasis. The aim of this work was to evaluate the plasma levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), total bilirubin (T. Bili), direct bilirubin (D. Bili), uric acid (UA), apolipoproteins (ApoA1 and ApoB), Lp(a) and activities of paraxonase 1 (PON1) in 100 patients with psoriasis and 100 controls, and to look for a correlation between these parameters in psoriasis. PON1, bilirubin and UA were measured spectrophotometrically, MDA by the high‐performance liquid chromatography method, apolipoproteins and Lp(a) by immunoprecipitation assays, and lipid and other biochemical parameters were determined by routine laboratory methods. In patients with psoriasis, there was a significant decrease in PON1, SOD and CAT activities (P < 0.05) and an increase in MDA levels (P < 0.01). Also, the levels of bilirubin (total and direct) and UA were decreased in patients with psoriasis but were not significant (P > 0.05). These results suggest that psoriasis was in a state of oxidative stress and that the protective effects of high‐density lipoprotein against atherosclerosis may be dependent on PON1 activity. Moreover, there is a negative correlation between antioxidant with Lp(a), apoB and MDA levels, suggesting that subjects with higher levels of Lp(a) and apoB and lower levels of antioxidant are more exposed to oxidative damage. These findings may explain in part the reported increase in cardiovascular mortality in psoriasis. Copyright © 2013 John Wiley & Sons, Ltd.     

Neuroprotective Effects of N-acetylcysteine on Experimental Closed Head Trauma in Rats

N-acetylcysteine (NAC) is a precursor of glutathione, a potent antioxidant, and a free radical scavenger. The beneficial effect of NAC on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of NAC on nervous system trauma remains less understood. Therefore, we aimed to investigate the therapeutic efficacy of NAC with an experimental closed head trauma model in rats. Thirty-six adult male Sprague–Dawley rats were randomly divided into three groups of 12 rats each: Group I (control), Group II (trauma-alone), and Group III (trauma+NAC treatment). In Groups II and III, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 2 h (Subgroups I-A, II-A, and III-A) and 12 h (Subgroups I-B, II-B, and III-B) after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. The closed head trauma significantly increased tissue malondialdehyde (MDA) levels (P<0.05), and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities (P<0.05), but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of NAC (150 mg/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels (P<0.05) and also significantly (P<0.05) increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the trauma-alone group, the neurons became extensively dark and degenerated into picnotic nuclei. The morphology of neurons in the NAC treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+NAC treatment groups. In conclusion, the NAC treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications.     

Genoprotection and genotoxicity of green tea (Camellia sinensis): Are they two sides of the same redox coin?

Abstract

Objectives

Regular intake of green tea associates with lower DNA damage and increased resistance of DNA to oxidant challenge. However, in vitro pro-oxidant effects of green tea have been reported. Both effects could be mediated by hydrogen peroxide (H₂O₂) which is generated by autoxidation of tea catechins. In large amounts, H₂O₂ is genotoxic, but low concentrations could activate the redox-sensitive antioxidant response element (ARE) via the Keap-1/Nrf2 redox switch, inducing genoprotective adaptations. Our objective was to test this hypothesis.

Methods

Peripheral lymphocytes from healthy volunteers were incubated for 30 minutes at 37°C in freshly prepared tea solutions (0.005, 0.01, 0.05%w/v (7, 14, 71 µmol/l total catechins) in phosphate buffered saline (PBS), with PBS as control) in the presence and absence of catalase (CAT). H₂O₂ in tea was measured colorimetrically. Oxidation-induced DNA lesions were measured by the Fpg-assisted comet assay.

Results

H₂O₂ concentrations in 0.005, 0.01, and 0.05% green tea after 30 minutes at 37°C were, respectively, ～3, ～7, and ～52 µmol/l. Cells incubated in 0.005 and 0.01% tea showed less (P < 0.001) DNA damage compared to control cells. Cells treated with 0.05% green tea showed ～50% (P < 0.001) more DNA damage. The presence of CAT prevented this damage, but did not remove the genoprotective effects of low-dose tea. No significant changes in expression of ARE-associated genes (HMOX1, NRF2, KEAP1, BACH1, and hOGG1) were seen in cells treated with tea or tea + CAT.

Conclusion

Genoprotection by low-dose green tea could be due to direct antioxidant protection by green tea polyphenols, or to H₂O₂-independent signalling pathways.     

Lipid peroxidation and some antioxidant enzymes in nasal polyp tissue

Nasal polyp (NP) is considered an inflammatory condition in nasal and paranasal sinus cavities and is frequently encountered in otolaryngology clinics. Although the pathophysiology of nasal polyps is poorly understood, it seems likely that the epithelium may play a critical role in the genesis of inflammatory nasal disease. The aim of this study was to investigate the role of free radicals and antioxidant enzymes in NP and compare these findings with concha bullosa (CB). NP and CB were obtained from 27 and 23 patients, respectively. Glutathione peroxidase (GSH-Px), catalase (CAT), xanthine oxidase (XO) total (enzymic plus non-enzymic) superoxide scavenger activity (TSSA), non-enzymic superoxide scavenger activity (NSSA), superoxide dismutase (SOD), and MDA levels in NP and CB were measured. GSH-Px activiy was significantly lower in patients with NP than in the CB group. However, CAT, XO activities and MDA levels were significantly higher in patients with NP than in the CB group, but TSSA, NSSA and SOD activities were unchanged. Increases in the levels of tissue MDA in patients with NP compared to the CB group may indicate the presence of free radical damage in patients with nasal NP.     

Adriamycin induced myocardial failure in rats: Protective role of Centella asiatica

Generation of reactive oxygen species and mitochondrial dysfunction has been implicated in adriamycin induced cardiotoxicity. Mitochondrial dysfunction is characterized by the accumulation of oxidized lipids, proteins and DNA, leading to disorganization of mitochondrial structure and systolic failure. The present study was aimed to evaluate the efficacy of Centella asiatica on the mitochondrial enzymes; mitochondrial antioxidant status in adriamycin induced myocardial injury. Adriamycin (2.5 mg/kg body wt., i.p.) induced mitochondrial damage in rats was assessed in terms of decreased activities (p< 0.05) of cardiac marker enzymes (lactate dehydrogenase, creatine phosphokinase, amino transferases), TCA cycle enzymes (isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, malate dehydrogenase, respiratory marker enzymes (NADH-dehydrogenase, cytochrome-C-oxidase), mitochondrial antioxidant enzymes (GPx, GSH, SOD,CAT) and increased (p< 0.05) level of lipid peroxidation. Mitochondrial damage was confirmed by transmission electron microscopic examination. Pre-co-treatment with aqueous extract of Centella asiatica (200 mg/kg body wt, oral) effectively counteracted the alterations in mitochondrial enzymes and mitochondrial defense system. In addition, transmission electron microscopy study confirms the restoration of cellular normalcy and accredits the cytoprotective role of Centella asiatica against adriamycin induced myocardial injury. Our results demonstrated elevated oxidative stress and mitochondrial dysfunction in adriamycin treated rats. Moreover, on the basis of our findings it may be concluded that the aqueous extract of C. asiatica not only possesses antioxidant properties but it may also reduce the extent of mitochondrial damage     

Guanidinoacetate Decreases Antioxidant Defenses and Total Protein Sulfhydryl Content in Striatum of Rats

Guanidinoacetate methyltransferase (GAMT) deficiency is an inherited neurometabolic disorder biochemically characterized by tissue accumulation of guanidinoacetate (GAA) and depletion of creatine. Affected patients present epilepsy and mental retardation whose pathogeny is unclear. In the present study we investigated the in vitro and in vivo (intrastriatal administration) effects of GAA on some oxidative stress parameters in rat striatum. Sixty-day-old rats were used for intrastriatal infusion of GAA. For the in vitro studies, 60-day-old Wistar rats were killed by decapitation and the striatum was pre-incubated for 1 h at 37°C in the presence of GAA at final concentrations ranging from 10 to 100 μM. Parameters of oxidative stress such as total radical-trapping antioxidant potential (TRAP), antioxidant enzymes (SOD, GPx, and CAT), protein carbonyl and thiol contents were measured. DNA damage was also evaluated. Results showed that GAA administration (in vivo studies) or the addition of 100 μM GAA to assays (in vitro studies) significantly decreased TRAP, SOD activity, and total thiol levels in rat striatum. In contrast, this guanidino compound did not alter protein carbonyl content and the activities of CAT and GPx. DNA damage was not found after intrastriatal administration of GAA. The data indicate that the metabolite accumulating in GAMT deficiency decreases antioxidant capacity and total thiol content in the striatum. It is therefore presumed that this pathomechanism may contribute at least in part to the pathophysiology of the brain injury observed in patients affected by GAMT deficiency.     

Oxidative damage and alterations in antioxidant enzyme activities in the kidneys of rat exposed to trichloroacetic acid: protective role of date palm fruit

In this study, we investigated the antioxidant and protective properties of date fruit aqueous extract (DFAE) on trichloroacetic acid (TCA)-induced nephrotoxicity in rat. Oral administration of TCA as drinking water (0.5 and 2 g/L) daily for 2 months caused nephrotoxicity as evident by elevated levels of plasma creatinine, urea, and uric acid. Activity of antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), was decreased, whereas superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were increased along with histopathological injuries. The oral administration of DFAE (4 mL/kg/day) to TCA-treated groups proved some significant correction by increasing the antioxidant activity of the CAT and GPx enzymes and normalizing the SOD activity and the MDA level (p?<?0.05). It also protected kidney's histology and normalized the functions of this organ. It could be concluded that DFAE has a protective role against TCA-induced oxidative stress in rat, thereby protecting the renal tissue from TCA-induced damage.     

Alterations in antioxidant enzymes and oxidative damage in experimental diabetic rat tissues: Effect of vanadate and fenugreek (Trigonella foenum graecum)

With the premise that oxygen free radicals may be responsible for the severity and complications of diabetes, the level of antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) as well as the oxidative damage were examined in the tissues of control, diabetic and treated rats. After three weeks of diabetes, the activity of CAT was significantly increased in heart in diabetes (about 6-fold) but decreased in liver. The SOD activity decreased significantly in liver but increased in brain. The activity of GPx decreased significantly in liver and increased in kidney. A significant increase was observed in oxidative damage in heart and kidney and a small increase in brain with decrease in liver and muscle. Vanadate and fenugreek (Trigonella foenum graecum) administration to diabetic animals showed a reversal of the disturbed antioxidant levels and peroxidative damage. Results suggest that oxidative stress play a key role in the complications of diabetes. Vanadate and fenugreek seeds showed an encouraging antioxidant property and can be valuable candidates in the treatment of the reversal of the complications of diabetes.     

Cyclosporine A induced changes to plasma and erythrocyte antioxidant defences

Abstract

Organ transplant recipients develop pronounced cardiovascular disease, and decreased antioxidant capacity in plasma and erythrocytes is associated with the pathogenesis of this disease. These experiments tested the hypothesis that the immunosuppressant cyclosporine A (CsA) alters erythrocyte redox balance and reduces plasma antioxidant capacity. Female Sprague-Dawley rats were randomly assigned to a control or CsA treated group. Treatment animals received 25 mg/kg/day of CsA via intraperitoneal injection for 18 days. Control rats were injected with the same volume of the vehicle. Three hours after the final CsA injection, rats were exsanguinated and plasma analysed for total antioxidant status (TAS), α-tocopherol, malondialdehyde (MDA), and creatinine. Erythrocytes were analysed for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glucose-6-phosphate dehydrogenase (G6PD) activities, α-tocopherol, and MDA. CsA administration resulted in a significant (P < 0.05) decrease in plasma TAS and significant increases (P < 0.05) in plasma creatinine and MDA. Erythrocyte CAT was significantly (P < 0.05) increased in CsA treated rats compared to controls. There were no significant differences (P > 0.05) in erythrocyte SOD, GPX, G6PD, α-tocopherol or MDA between groups. In summary, CsA alters erythrocyte antioxidant defence and decreases plasma total antioxidant capacity.     

Modulation of antioxidant defence system in brain of rainbow trout (Oncorhynchus mykiss) after chronic carbamazepine treatment

We investigated the effect of long-term exposure to CBZ on the antioxidant system in brain tissue of rainbow trout. Fish were exposed to sublethal concentrations of CBZ (1.0 μg/L, 0.2 mg/L or 2.0 mg/L) for 7, 21, and 42 days. Oxidative stress indices (LPO and CP) and activities of antioxidant enzymes (SOD, CAT, GPx and GR) in fish brain were measured. In addition, non-enzymatic antioxidant (GSH) was determined after 42 days exposure. Carbamazepine exposure at 0.2 mg/L led to significant increases (p < 0.05) of LPO and CP after 42 days and, at 2.0 mg/L, after 21 days. Activities of the antioxidant enzymes SOD, CAT, and GPx in CBZ-treated groups slightly increased during the first period (7 days). However, activities of all measured antioxidant enzymes were significantly inhibited (p < 0.05) at 0.2 mg/L exposure after 42 days and after 21 days at 2.0 mg/L. After 42 days, the content of GSH in fish brain was significantly lower (p < 0.05) in groups exposed to CBZ at 0.2 mg/L and 2.0 mg/L than in other groups. Prolonged exposure to CBZ resulted in excess reactive oxygen species formation, finally resulting in oxidative damage to lipids and proteins and inhibited antioxidant capacities in fish brain. In short, a low level of oxidative stress could induce the adaptive responses of antioxidant enzymes, but long-term exposure to CBZ could lead to serious oxidative damage in fish brain.     

Determining oxidant and antioxidant status in patients with genital warts

Abstract

Objectives

Warts are abnormal skin growths caused by human papilloma virus (HPV) infections within the skin of patients. Genital warts usually appear in the perianal and perigenital regions. Asymptomatic warts may be activated after years and may damage natural immunity. The inflammation that occurs during this process may lead to an imbalance between the prooxidant and the antioxidant systems. The aim of this study was to investigate erythrocyte glutathione peroxidase (GSH-Px) activity, serum paraoxonase enzyme levels, and oxidative stress levels in patients with genital warts.

Patients and Methods

In total, 32 patients with genital warts and 35 healthy subjects were included in this study. Erythrocyte GSH-Px activity, serum catalase activity, and paraoxonase enzyme, and malondialdehyde (MDA) levels were determined.

Results

Erythrocyte GSH-Px activity, serum MDA levels, and catalase activity were significantly higher in patients with genital warts than in controls (P < 0.01, P < 0.05, and P < 0.05, respectively). However, serum paraoxonase enzyme levels were not significantly different between groups (P > 0.05). Serum triglyceride levels were significantly lower in patients with genital warts than in controls (P < 0.01). However, there were no statistically signi?cant differences between groups with respect to total cholesterol, high-density lipoprotein cholesterol, or low-density lipoprotein cholesterol levels (all P > 0.05).

Conclusions

Our data suggest that oxidative stress is increased in genital warts. Increased oxidative stress levels may contribute to the pathogenesis of genital warts, and prolonged HPV infection due to chronic inflammation could also affect oxidative stress.     

Acute and Chronic Hyperammonemia Modulate Antioxidant Enzymes Differently in Cerebral Cortex and Cerebellum

Studies on acute hyperammonemic models suggest a role of oxidative stress in neuropathology of ammonia toxicity. Mostly, a low grade chronic type hyperammonemia (HA) prevails in patients with liver diseases and causes derangements mainly in cerebellum associated functions. To understand whether cerebellum responds differently than other brain regions to chronic type HA with respect to oxidative stress, this article compares active levels of all the antioxidant enzymes vis a vis extent of oxidative damage in cerebral cortex and cerebellum of rats with acute and chronic HA induced by intra-peritoneal injection of ammonium acetate (successive doses of 10 × 10³ & 8 × 10³ μmol/kg b.w. at 30 min interval for acute and 8 × 10³ μmol/kg b.w. daily up to 3 days for chronic HA). As compared to the respective control sets, cerebral cortex of acute HA rats showed significant decline (P < 0.01–0.001) in the levels of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) but with no change in glutathione reductase (GR). In cerebellum of acute HA rats, SOD, catalase and GR though declined significantly, GPx level was found to be stable. Contrary to this, during chronic HA, levels of SOD, catalase and GPx increased significantly in cerebral cortex, however, with a significant decline in the levels of SOD and GPx in cerebellum. The results suggest that most of the antioxidant enzymes decline during acute HA in both the brain regions. However, chronic HA induces adaptive changes, with respect to the critical antioxidant enzymes, in cerebral cortex and renders cerebellum susceptible to the oxidative stress. This is supported by ∼ 2- and 3-times increases in the level of lipid peroxidation in cerebellum during chronic and acute HA respectively, however, with no change in the cortex due to chronic HA.     

Erythrocyte caspase-3 and antioxidant defense is activated in red blood cells and plasma of type 2 diabetes patients at first clinical onset

Abstract

Objectives

We studied erythrocyte (RBC) caspase-3 activity and oxidative status in plasma and RBCs of 33 patients with type 2 diabetes at first clinical onset and 23 age-matched non-diabetes control subjects.

Methods

Caspase-3 activity was assayed during the life span of RBCs; lipid peroxides and total antioxidant capacity (TEAC) were assessed in plasma and RBCs as indicators of oxidative stress and non-enzymatic antioxidant defense; and superoxide dismutase, catalase, and glutathione peroxidase activity were measured in RBCs as enzymatic antioxidants.

Results

We found that, compared to controls, RBCs caspase-3 is activated early in type 2 diabetes (P < 0.05); TEAC and malondialdehyde increased in plasma of patients with early diabetes, even when hypertension and macroangiopathy were present (P < 0.01); and RBCs TEAC, malondialdehyde (P < 0.01), superoxide dismutase, and glutathione peroxidase (P < 0.05) exhibited similar behavior in patients with diabetes and hypertensive patients with diabetes.

Discussion

Increased antioxidant defense in plasma and RBCs of early type 2 diabetes patients is a potential mechanism that can overcome oxidative damage induced by reactive oxygen species overproduction, and occurs even in RBCs with a decreased life span. This observation could provide a possible explanation for the controversial effects of antioxidant supplementation in diabetes patients.     

Co- and Post-Treatment with Lysine Protects Primary Fish Enterocytes against Cu-Induced Oxidative Damage

The aim of the work was primarily to explore the protective activity pathways of lysine against oxidative damage in fish in vivo and in enterocytes in vitro. First, grass carp were fed diets containing six graded levels of lysine (7.1–19.6 g kg^-1 diet) for 56 days. Second, the enterocytes were treated with different concentrations of lysine (0–300 mg/L in media) prior to (pre-treatment), along with (co-treatment) or following (post-treatment) with 6 mg/L of Cu for 24 h. The results indicated that lysine improved grass carp growth performance. Meanwhile, lysine ameliorated lipid and protein oxidation by elevating the gene expression and activity of antioxidant enzymes (superoxide dismutase (SOD), glutathioneperoxidase (GPx), glutathione-S-transferase (GST) and reductase (GR)), and nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA levels in fish intestine. The in vitro studies showed that co- and post-treatment with lysine conferred significant protection against Cu-induced oxidative damage in fish primary enterocytes as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) OD values, along with alkaline phosphatase (ALP) and lactate dehydrogenase activities, and the depletion of protein carbonyl (PC), malondialdehyde (MDA) and 8-hydroxydeoxyguanosine contents. Moreover, lysine co-treatment decreased the activities and mRNA level of cellular SOD, GPx, GST and GR compared with the Cu-only exposed group. Gene expression of the signalling molecule Nrf2 showed the same pattern as that of SOD activity, whereas Kelch-like ECH-associated protein 1b (Keap1b) followed the opposite trend, indicating that co-treatment with lysine induced antioxidant enzymes that protected against oxidative stress through Nrf2 pathway. In addition, post-treatment with lysine increased proteasomal activity and blocked the Cu-stimulated increase in mRNA levels of GST and associated catalase (CAT) and GST activities (P<0.01 and P<0.001). GR activity and gene expression, and glutathione (GSH) content followed an opposite trend to GST activity (P<0.05). Thus, post-treatment of lysine elevated protein and DNA repair abilities and ameliorated the cellular redox state of enterocytes. The overall results suggest that lysine plays a significant role in the protection of fish intestine in vivo and in vitro through the induction of key antioxidant protection.     

Lead-induced increase in antioxidant enzymes and lipid peroxidation products in developing rat brain

Pregnant rats were treated with 0.4% lead acetate through drinking water from 6th day of gestation and this treatment was continued till 21 post natal days (PND). Four regions of the brain namely hippocampus, cerebellum, frontal cortex and brain stem were dissected at 10, 20, 30 and 40 PND for estimation of lipid peroxidation products (LPP), catalase (CAT) and superoxide dismutase (SOD). The results indicate that there was a significant (P < 0.05) increase of LPP in exposed rats than their corresponding control at 10, 20 and 30 PND both in hippocampus and cerebellum. At PND 40, the LPP of control and exposed were found to be almost same in both the tissues indicating recovery from lead toxicity. CAT activity was significantly (P < 0.05) high in hippocampus of exposed rats up to PND 30 but up to PND 20 in cerebellum and frontal cortex. However, in brain stem, a significant (P < 0.05) increase in CAT activity was observed only at PND 10. A significant (P < 0.05) increase in SOD activity was observed up to PND 30 both in hippocampus and cerebellum on lead exposure. Frontal cortex exhibited a similar significant (P < 0.05) increase of SOD activity up to PND 20 and for brain stem up to PND 10. There was no significant change in the activity of antioxidant enzymes (CAT and SOD) and LPP in all the four brain tissues of control and exposed rats at PND 40 indicating recovery from lead-induced oxidative stress. This research work was presented as a poster in Annual Biomedical Research Conference for Minority Students (ABRCMS) at Dallas, Texas, USA, during November 10–13, 2004 and the abstract was printed on page 231 of the Conference Proceedings     

Oxidative stress and antioxidant defenses in pregnant women

Abstract

Objectives

Oxidative stress (OS) is defined as an imbalance in the production of reactive oxygen species and the capacity of antioxidant defenses. The objective of this work was to investigate OS and antioxidant capacity in pregnant women.

Methods

Parameters of the oxidative status and antioxidant capacity in serum and whole blood were evaluated in thirty-nine women with normal pregnancy.

Results

The assessment of antioxidants indicated an increase in superoxide dismutase and catalase activities (P < 0.05 and P < 0.01) and a decrease in ascorbic acid levels and the total content of sulfhydryl (P < 0.05 and P < 0.001). Additionally, when the pro-oxidant system was investigated we found an increase (P < 0.01) in malondialdehyde and no significant change (P > 0.05) in protein carbonylation.

Discussion

This study demonstrates that there is a change in the pro-oxidant and antioxidant defenses associated with body and circulation changes that are inherent to the pregnancy process.     

Longevity and antioxidant enzymes,non-enzymatic antioxidants and oxidative stress in the vertebrate lung: a comparative study

It has been proposed that antioxidants can be longevity determinants in animals. However, no comprehensive study has been conducted to try to relate free radicals with maximum life span. This study compares the lung tissue of various vertebrate species — amphibia, mammals and birds — showing very different and well known maximum life spans and life energy potentials. The lung antioxidant enzymes superoxide dismutase, catalase, Se-dependent and non-Se-dependent glutathione peroxidases, and glutathione reductase showed significantly negative correlations with maximum life span. The same was observed for the lung antioxidants, reduced glutathione and ascorbate. It is concluded that a generalized decrease in tissue antioxidant capacity is a characteristic of longevous species. It is suggested that a low rate of free radical recycling (free-radical generation and scavenging) can be an important factor involved in the evolution of high maximum animal longevities. A low free-radical production could be responsible for a low rate of damage at critical sites such as mitochondrial DNA.Abbreviations CAT catalase - COX cytochrome oxidase - GPx glutathione peroxidase - GR glutathione reductase - GSH reduced glutathione - GSSG oxidized glutathione - LEP life energy potential - MDA malondialdehyde - MLSP maximum life span - MR metabolic rate - MW molecular weight - PO₂ partial pressure of oxygen - SOD superoxide dismutase - VO₂ basal oxygen consumption     

Effect of acetone extract from stem bark of Acacia species (A. dealbata,A. ferruginea and A. leucophloea) on antioxidant enzymes status in hydrogen peroxide-induced HepG2 cells

Acacia species are multipurpose trees, widely used in the traditional systems of medicine to treat various ailments. The major objective of the present study was to determine the gene expression of enzymatic antioxidants by acetone extract from the stem bark of three Acacia species (Acacia dealbata, Acacia ferruginea and Acacia leucophloea) in hydrogen peroxide (H₂O₂)-induced human hepatoma (HepG2) cells. The expression of antioxidant enzymes such as superoxide dismutase containing copper–zinc (CuZnSOD)/manganese (MnSOD), catalase (CAT) and glutathione peroxidase (GPx) in HepG2 cells was evaluated by real-time PCR. The results of antioxidant enzyme expression in real-time PCR study revealed that the H₂O₂ (200 μM) challenged HepG2 cells reduced the expression of enzymes such as SOD, GPx and CAT. However, the cells pre-treated with acetone extracts of all the three Acacia species significantly (P > 0.05) up-regulated the expression of antioxidant enzymes in a concentration dependent manner (25, 50 and 75 μg/mL). In conclusion, the findings of our study demonstrated that the acetone extract of Acacia species effectively inhibited H₂O₂ mediated oxidative stress and may be useful as a therapeutic agent in preventing oxidative stress mediated diseases.