Catalase Abstracts 2

© 2011

Beneficial effects of vitamin C and vitamin E on reserpine-induced oral dyskinesia in rats: critical role of striatal catalase activity

            (Faria, Abilio et al. 2005) Download

Oral dyskinesias are implicated in a series of neuropathologies and have been associated to an increase in oxidative stress. Several antioxidants, including vitamin E, decrease reserpine-induced oral dyskinesia (OD) in rodents and we have described a protective role of striatal catalase against the development of OD. The aim of this study was to verify the effects of vitamin C alone or in combination with vitamin E on reserpine-induced OD as well as to determine a possible role of catalase in the antidyskinetic property of these vitamins. Different doses of vitamin C attenuated reserpine-induced increase in OD. A similar treatment with an effective dose of vitamin C concomitant to an effective dose of vitamin E potentiated the antidyskinetic effect of both vitamins when administered alone. The administration of these vitamins alone produced an increase in striatal catalase activity that likewise was potentiated by their combined administration. In addition, the antidyskinetic property of vitamin E and vitamin C was abolished by a concomitant treatment with the catalase inhibitor aminotriazole. These results indicate a beneficial effect of these vitamins and reinforce the critical role of striatal catalase against the development of oral dyskinesias.

Catalase: a tetrameric enzyme with four tightly bound molecules of NADPH

            (Kirkman and Gaetani 1984) Download

Catalases (H2O2:H2O2 oxidoreductase, EC 1.11.1.6) from many species are known to be tetramers of 60,000-dalton subunits, with four heme groups per tetramer. Previous authors have determined the amino acid sequence and three-dimensional structure of bovine liver catalase. Studies of the regulation of the pentose phosphate pathway led the present authors to a search for proteins that bind NADP+ and NADPH in human erythrocytes. An unexpected result of that search was the finding that a major reservoir of bound NADPH in human erythrocytes is catalase. Each tetrameric molecule of human or bovine catalase contains four molecules of tightly bound NADPH. The binding sites have the relative affinities NADPH greater than NADH greater than NADP+ greater than NAD+. NADPH does not seem to be essential for the enzymic conversion of H2O2 to O2 and water but does provide protection of catalase against inactivation by H2O2.

Catalase activity, serum trace element and heavy metal concentrations, and vitamin A, D and E levels in pre-eclampsia

            (Kolusari, Adali et al. 2009) Download

PURPOSE OF INVESTIGATION: In this study we aimed to measure the activity of catalase, which is an antioxidant enzyme, the concentrations of some trace elements and heavy metals, and vitamin A, D and E levels in serum samples of patients with hydatidiform mole, normal pregnancies and healthy non pregnant women. METHODS: Seventy-two women were enrolled in this study. Of these, 24 were healthy women in the first trimester of pregnancy (HP), 24 were healthy non-pregnant women (NP) and 24 were patients with complete hydatidiform mole (CHM). RESULTS: Serum levels of catalase, Zn, Co, vitamin A, D and E were significantly lower in the CHM group when compared with the HP and NP groups (p < 0.001). Serum levels of Cu, Fe, and Cd were significantly higher in the CHM group when compared with the HP and NP groups (p < 0.001). CONCLUSION: The assessment of oxidant/antioxidant imbalance in pregnant women could be useful in the early determination of molar pregnancy and supplementation with antioxidants may be useful in the treatment of CHM, and may prevent recurrent molar pregnancy.

Caspase-8 dependent TRAIL-induced apoptosis in cancer cell lines is inhibited by vitamin C and catalase

            (Perez-Cruz, Carcamo et al. 2007) Download

TNF-related apoptosis-inducing ligand (TRAIL/ Apo-2L) is a member of the TNF family of apoptosis-inducing proteins that initiates apoptosis in a variety of neoplastic cells while displaying minimal or absent cytotoxicity to most normal cells. Therefore, TRAIL is currently considered a promising target to develop anti-cancer therapies. TRAIL-receptor ligation recruits and activates pro-caspase-8, which in turn activates proteins that mediate disruption of the mitochondrial membranes. These events lead to the nuclear and cytosolic damage characteristic of apoptosis. Here we report that TRAIL-induced apoptosis is mediated by oxidative stress and that vitamin C (ascorbic acid), a potent nutritional antioxidant, protects cancer cell lines from apoptosis induced by TRAIL. Vitamin C impedes the elevation of reactive oxygen species (ROS) levels induced by TRAIL and impairs caspase-8 activation. We found that the removal of hydrogen peroxide by extracellular catalase during TRAIL-induced apoptosis also impairs caspase-8 activation. These data suggest that hydrogen peroxide is produced during TRAIL-receptor ligation, and that the increase of intracellular ROS regulates the activation of caspase-8 during apoptosis. Additionally we propose a mechanism by which cancer cells might resist apoptosis via TRAIL, by the intake of the nutritional antioxidant vitamin C.

Vitamin A supplementation induces a prooxidative state in the striatum and impairs locomotory and exploratory activity of adult rats

            (de Oliveira, de Bittencourt Pasquali et al. 2007) Download

Although vitamin A has been reported to be essential to brain homeostasis, some central nervous system (CNS)-associated deleterious effects may be induced by vitamin A or by its metabolites. In this work, we investigated the effects of acute and chronic vitamin A supplementation at therapeutic (1,000 or 2,500 IU/kg/day) or excessive (4,500 or 9,000 IU/kg/day) doses on the redox state of the rat striatum. We found a 1.8- to 2.7-fold increase of lipid peroxidation in the striatum after acute or chronic supplementation (TBARS method). Therapeutic doses induced a 1.6- to 2.2-fold increase of protein carbonylation (dinitrophenylhydrazine (DNPH) derivatization). Vitamin A supplementation induced a 1.2- to 1.4-fold decrease of protein thiol content acutely and chronically. Superoxide dismutase (SOD) activity, assessed through the inhibition of epinephrine's autoxidation, was increased in a dose-dependent manner chronically. Acutely, both therapeutic and excessive vitamin A doses induced a 1.8- to 2.2-fold decrease of catalase (CAT) activity, as determined through the rate of decrease of hydrogen peroxide (H(2)O(2)). Glutathione peroxidase (GPx) activity did not change in this experimental model. Some vitamin A doses decreased the non-protein thiol content only chronically. Vitamin A supplementation decreased the striatal non-enzymatic antioxidant defenses (TRAP assay). Furthermore, our results show that vitamin A supplementation impaired the SOD/CAT ratio. Moreover, we observed a 1.6- to 2.0-fold decrease of locomotion and exploration in an open field after vitamin A supplementation. Therefore, our results suggest that vitamin A supplementation induces oxidative stress in the rat striatum and that it may be related to a metabolic impairment in such brain area.

Therapeutic vitamin A doses increase the levels of markers of oxidative insult in substantia nigra and decrease locomotory and exploratory activity in rats after acute and chronic supplementation

            (de Oliveira, Silvestrin et al. 2008) Download

Vitamin A is known to regulate some central nervous system (CNS)-associated functions. Vitamin A at high doses has been demonstrated to be beneficial in the treatment of some diseases, for instance acute promyelocytic leukemia. However, vitamin A and its naturally occurring metabolites (retinoids) are known to alter neuronal function, inducing behavioral disorders. Here we provide an evidence to indicate that vitamin A supplementation, at both therapeutic and excessive doses, induces oxidative stress in the rat substantia nigra. Vitamin A supplementation induced lipid peroxidation, protein carbonylation, and oxidation of protein thiol groups, as well as change in catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activity. Surprisingly, locomotory and exploratory activity of rats were decreased after acute and chronic vitamin A supplementation. Therefore, we may conclude from our results that vitamin A supplementation is prooxidant to the rat substantia nigra and effective in altering behavior.


References

de Oliveira, M. R., M. A. de Bittencourt Pasquali, et al. (2007). "Vitamin A supplementation induces a prooxidative state in the striatum and impairs locomotory and exploratory activity of adult rats." Brain Res 1169: 112-9.

de Oliveira, M. R., R. B. Silvestrin, et al. (2008). "Therapeutic vitamin A doses increase the levels of markers of oxidative insult in substantia nigra and decrease locomotory and exploratory activity in rats after acute and chronic supplementation." Neurochem Res 33(3): 378-83.

Faria, R. R., V. C. Abilio, et al. (2005). "Beneficial effects of vitamin C and vitamin E on reserpine-induced oral dyskinesia in rats: critical role of striatal catalase activity." Neuropharmacology 48(7): 993-1001.

Kirkman, H. N. and G. F. Gaetani (1984). "Catalase: a tetrameric enzyme with four tightly bound molecules of NADPH." Proc Natl Acad Sci U S A 81(14): 4343-7.

Kolusari, A., E. Adali, et al. (2009). "Catalase activity, serum trace element and heavy metal concentrations, vitamin A, vitamin D and vitamin E levels in hydatidiform mole." Clin Exp Obstet Gynecol 36(2): 102-4.

Perez-Cruz, I., J. M. Carcamo, et al. (2007). "Caspase-8 dependent TRAIL-induced apoptosis in cancer cell lines is inhibited by vitamin C and catalase." Apoptosis 12(1): 225-34.