Evaluation of antioxidant therapy in experimental Chagas disease

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Abstract

Abstract INTRODUCTION: Stimulation of inflammatory mediators such as cytokines and chemokines may cause oxidative stress in Chagas disease. In this study, we evaluated the merit of vitamins C and E as antioxidant therapy to minimize the oxidative stress-induced damage in an experimental model of Chagas disease. METHODS: Ninety-six Swiss mice were infected with Trypanosoma cruzi QM2 and treated with vitamins C, E, or both (C/E) for 60 and 120 days, and their effects compared to placebo administration were evaluated in the acute and chronic disease phases. RESULTS: There was no difference in parasitemia among treatment groups. However, histological analysis showed more severe inflammation in the skeletal muscle in the vitamin supplementation groups at both the acute and chronic phases. Biochemical analyses during the acute phase showed increased ferric-reducing ability of plasma (FRAP) and glutathione (GSH) levels in the vitamin C and C/E groups. In the chronic phase, a decrease in GSH levels was observed in the vitamin E group and a decrease in thiobarbituric acid reactive substances (TBARS) was observed in the vitamin C/E group. Moreover, there was a decrease in TBARS in the cardiac tissues of the vitamin C and C/E groups compared to that of the placebo group, although this level was greater in the vitamin E group than in the vitamin C group. CONCLUSIONS: The antioxidant action of vitamins C and E reduced oxidative stress in both the acute and chronic phases of Chagas disease, with a marked effect from joint administration, indicating their inherent synergism.

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Free Radicals in Biology: Oxidative Stress and the Effects of Ionizing Radiation

P.A. Riley (2009)

The most important electron acceptor in the biosphere is molecular oxygen which, by virtue of its bi-radical nature, readily accepts unpaired electrons to give rise to a series of partially reduced species collectively known as reduced (or 'reactive') oxygen species (ROS). These include superoxide (O.2-), hydrogen peroxide (H2O2), hydroxyl radical (HO.) and peroxyl (ROO.) and alkoxyl (RO.) radicals which may be involved in the initiation and propagation of free radical chain reactions and which are potentially highly damaging to cells. Mechanisms have evolved to restrict and control such processes, partly by compartmentation, and partly by antioxidant defences such as chain-breaking antioxidant compounds capable forming stable free radicals (e.g. ascorbate, alpha-tocopherol) and the evolution of enzyme systems (e.g. superoxide dismutase, catalase, peroxidases) that diminish the intracellular concentration of the ROS. Although some ROS perform useful functions, the production of ROS exceeding the ability of the organism to mount an antioxidant defence results in oxidative stress and the ensuing tissue damage may be involved in certain disease processes. Evidence that ROS are involved in primary pathological mechanisms is a feature mainly of extraneous physical or chemical perturbations of which radiation is perhaps the major contributor. One of the important radiation-induced free-radical species is the hydroxyl radical which indiscriminately attacks neighbouring molecules often at near diffusion-controlled rates. Hydroxyl radicals are generated by ionizing radiation either directly by oxidation of water, or indirectly by the formation of secondary partially ROS. These may be subsequently converted to hydroxyl radicals by further reduction ('activation') by metabolic processes in the cell. Secondary radiation injury is therefore influenced by the cellular antioxidant status and the amount and availability of activating mechanisms. The biological response to radiation may be modulated by alterations in factors affecting these secondary mechanisms of cellular injury.

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Vitamin C in human health and disease is still a mystery ? An overview

K Akhilender Naidu (2003)

Ascorbic acid is one of the important water soluble vitamins. It is essential for collagen, carnitine and neurotransmitters biosynthesis. Most plants and animals synthesize ascorbic acid for their own requirement. However, apes and humans can not synthesize ascorbic acid due to lack of an enzyme gulonolactone oxidase. Hence, ascorbic acid has to be supplemented mainly through fruits, vegetables and tablets. The current US recommended daily allowance (RDA) for ascorbic acid ranges between 100–120 mg/per day for adults. Many health benefits have been attributed to ascorbic acid such as antioxidant, anti-atherogenic, anti-carcinogenic, immunomodulator and prevents cold etc. However, lately the health benefits of ascorbic acid has been the subject of debate and controversies viz., Danger of mega doses of ascorbic acid? Does ascorbic acid act as a antioxidant or pro-oxidant ? Does ascorbic acid cause cancer or may interfere with cancer therapy? However, the Panel on dietary antioxidants and related compounds stated that the in vivo data do not clearly show a relationship between excess ascorbic acid intake and kidney stone formation, pro-oxidant effects, excess iron absorption. A number of clinical and epidemiological studies on anti-carcinogenic effects of ascorbic acid in humans did not show any conclusive beneficial effects on various types of cancer except gastric cancer. Recently, a few derivatives of ascorbic acid were tested on cancer cells, among them ascorbic acid esters showed promising anticancer activity compared to ascorbic acid. Ascorbyl stearate was found to inhibit proliferation of human cancer cells by interfering with cell cycle progression, induced apoptosis by modulation of signal transduction pathways. However, more mechanistic and human in vivo studies are needed to understand and elucidate the molecular mechanism underlying the anti-carcinogenic property of ascorbic acid. Thus, though ascorbic acid was discovered in 17th century, the exact role of this vitamin/nutraceutical in human biology and health is still a mystery in view of many beneficial claims and controversies.

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Antioxidants, tissue damage, and endurance in trained and untrained young male rats.

Charles Venditti, S Meo (1996)

It is well known that physical training permits an animal to respond successfully to exercise loads of various types, intensities, and durations. Furthermore, the trained animal can sustain the activity for a long period before the fatigue becomes limiting. The effects of physical training on the antioxidant defenses of tissues and on their susceptibility to damage induced by exhaustive exercise have been investigated. Therefore, untrained rats were sacrificed either at rest or immediately after swimming to exhaustion. Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest or after exhaustive swimming. Homogenates of liver, heart, and muscle were used for biochemical determinations. Mitochondrial and sarcoplasmic (SR) or endoplasmic (ER) reticulum integrity was assessed with measurements of respiratory control index and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on the antioxidant protection systems of tissues was examined by determining the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity. Mitochondrial, SR, and ER integrity and lipid peroxidation were similar in trained and untrained at rest animals, whereas the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity of tissues were greater in trained animals. The exhaustive exercise gave rise to tissue damage irrespective of the trained state, as documented by similar loss of SR and ER integrity, and by increase in lipid peroxidation found in exhausted trained and untrained rats. Because exercise endurance capacity was greatly increased by training, our results suggest that free radical-induced damage in muscle could be one of the factors terminating muscle effort. In effect, the greater antioxidant level should allow trained muscle to withstand oxidative processes more effectively, thus lengthening the time required so that the cell function is sufficiently damaged as to make further exercise impossible.