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Inflammation, particularly low-grade chronic inflammation, appears to affect several brain functions, from early brain development to the development of neurodegenerative disorders and perhaps some psychiatric diseases. On the other hand, nutrition and dietary components and patterns have a plethora of anti- and pro-inflammatory effects that could be linked to cognitive function. Even a modest effect of nutrition on cognitive decline could have significant implications for public health. This paper summarizes the available evidence regarding inflammation as a key mechanism in cognitive function and nutritional pro- or anti-inflammatory effects with the purpose of linking the apparent disparate disciplines of nutrition, immunity, and neurology. [ABSTRACT FROM AUTHOR]

This paper will review our recent data relevant to the antioxidant effects of N-acetylserotonin (NAS), the immediate precursor of melatonin, the pineal gland indole. Mechanisms of the antioxidant effects of NAS might involve interaction with melatonin type 3 receptors and nonreceptor mechanisms such as stimulation of glutathione peroxidase, an antioxidant enzyme; inhibition of lipid peroxidation; suppression of phospholipase A2 activation; attenuation of tumor necrosis factor-α production; prevention of pathological opening of the mitochondrial permeability transition pores; and inhibition of sepiapterin reductase, the key enzyme of biosynthesis of tetrahydrobiopterin, the essential cofactor of nitric oxide synthase. NAS actions on some of these enzymes might be receptor-mediated. Protective effects of NAS against oxidative damage are independent from the effect of melatonin and, depending on the model, are 5 to 20 times stronger than that of melatonin. Antioxidant effect of NAS might underpin its cognition-enhancing, antiaging, antidepressant, antihypertensive, and antitumor effects. NAS and its derivatives might be useful in protection against oxidative stress-related disorders (cell death, mutagenesis, aging) and diseases (sepsis, cancer, postischemic trauma, Alzheimer's disease, parkinsonism). [ABSTRACT FROM AUTHOR]

We have studied the activities of antioxidant enzymes (AOE), namely, copper-zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD), and catalase (CAT), and the activity of catecholaminedegrading enzyme monoamine oxidase (MAO) and uncoupling protein 1 (UCP1) content in brown fat (BF) of hypo- and hyperthyroid rats. We found that hypothyroidism decreased BF UCP1 content and increased MAO, MnSOD, and CAT activities. T3 increased UCP1 content and MnSOD activity and decreased CuZnSOD, MAO, and CAT activities, while T4 significantly altered (decreased) only CAT activity. This study shows that UCP1 content and MAO and AOE activities in rat BF are notably affected by changed thyroid status. [ABSTRACT FROM AUTHOR]

Most aquatic organisms behave as conformers with respect to environmental variables, including changes in O2 availability. Aquatic species that show tolerance to hypoxia/anoxia or hyperoxia can be excellent models for investigating physiological and biochemical adaptations that deal with changing O2 and consequent changes in metabolic rate and production of reactive oxygen species (ROS). Here, I summarize selected data on ROS production and antioxidant defenses in a model marine invertebrate, the bivalve Mytilus, under different environmental and physiological conditions. An example of other bivalves adapted to particular environments (the Antarctic Sea) is also reported. These studies contributed to the knowledge on pro-oxidant and antioxidant processes in aquatic invertebrates from comparative and environmental perspectives. A common role for metallothioneins in antioxidant protection in mammals and aquatic invertebrates is underlined in different conditions, from human disease to responses to environmental exposure to heavy metals. [ABSTRACT FROM AUTHOR]

Results of most epidemiological and laboratory studies suggest an inverse relationship between regular exercise and the risk of certain malignancies, such as intestinal, colon, pancreatic, breast, lung, skin, mammary, endometrial, and prostate cancer. However, physical activity can have different influence on carcinogenesis, depending on energy supply and the age of the subject as well as strength, frequency, and length of exercise. The biochemical and molecular basis of the interaction between aerobic physical activity and tumorigenic processes remains poorly understood. Physical activity may generate reactive oxygen species (ROS) to a different extent. Mild oxidative stress caused by moderate physical activity can activate cellular stress response signaling and potentiate cellular antioxidant defense capacity. However, accumulation of relatively large amounts of ROS as a consequence of exhaustive exercise can either directly damage DNA, causing mutation, or promote tumorigenesis by activating proinflammatory signaling. This review highlights the effects of physical activity on various malignancies in the context of redox status modulated during exercise. [ABSTRACT FROM AUTHOR]

The chemopreventive agent sulforaphane is an isothiocyanate derived from cruciferous vegetables. Transcriptional activation of antioxidant response element (ARE)-regulated phase II detoxification and antioxidant genes through the induction of transcription factor NF-E2-related factor-2 (Nrf2) is considered as the prime mechanism of its chemopreventive action. Cellular level of Nrf2 is tightly regulated by proteolysis through Cullin3 (Cul3)/Kelch-like ECH-associated protein 1 (Keap1)-dependent polyubiquitination. Sulforaphane is an electrophile that can react with protein thiols to form thionoacyl adducts and is believed to affect the Cys residues in Keap1 protein. In addition, sulforaphane might affect the activity of a variety of intracellular kinases to phosphorylate Nrf2 proteins, which dictates the nucleocytoplasmic trafficking of Nrf2 or modulates the Nrf2 protein stability. This review is designed to briefly account for the regulatory mechanism of Nrf2 protein expression by Cul3/Keap1 E3 ligase and for the possible roles of posttranslational modifications of cellular Keap1 or Nrf2 proteins by sulforphane in the regulation of ARE-dependent gene activation. [ABSTRACT FROM AUTHOR]

In a placebo-controlled double-blinded study, the effect of 8 weeks of grape juice was compared to the effect of isocaloric placebo juice. Volunteers with a systolic blood pressure > 130 mmHg and diastolic blood pressure > 90 mmHg were recruited. A total of 40 healthy subjects were randomized to receive isocaloric juices for 8 weeks. Twenty-one subjects were instructed to consume 5.5 mL/kg daily of grape juice (GJ), and 19 subjects consumed placebo juice (PJ). Plasma antioxidant vitamin C, total radical trapping antioxidant capacity, blood pressure, and lymphocyte DNA damage were assessed pre- and postsupplementation. Plasma total radical-trapping antioxidant potential showed an increase at the level of 1.31 ± 0.01 (postsupplementation) versus 1.33 ± 0.01 (presupplementation) ( P < 0.1). Grape juice consumption resulted in a 26% decrease in lymphocyte DNA (both hydrogen peroxide treated or spontaneous) in the grape juice group, while no difference was found in the PJ group. Consuming moderate amounts of daily grape juice may favorably affect antioxidant defense systems and lymphocyte DNA damage in hypertensive individuals. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is characterized by fasting hyperglycemia, with both type 1 and type 2 diabetes. Persons are also known to be prone to develop complications related to elevated blood glucose concentrations, including atherosclerosis, retinal damage, cataract, and neuropathy. Hyperglycemia may also result in increased production of the reactive oxygen species within numerous biochemical pathways that have the potential to initiate changes in endothelial function. This article demonstrates the presence of lipid peroxidation products in the red cell membranes of type 2 diabetic patients compared to the normal subjects. These membranes are more susceptible to exogenous oxidative stress than those of normal healthy individuals. Significantly higher activities of antioxidant enzymes, namely, serum peroxidase, superoxide dismutase (SOD), and catalase (CAT) were found in type 2 diabetic patients as compared to control. This study led us to conclude that elevated levels of glucose induce oxidative stress that is ultimately reflected by the increased malondialdehyde (MDA) levels in erythrocyte ghost membranes of diabetic patients. Hyperglycemia also induced an increase in antioxidant enzymes and a relationship seems to exist between diabetic complications and elevated levels of these enzymes. It is suggested that these antioxidant enzymes may be considered as markers for vascular injury. [ABSTRACT FROM AUTHOR]

Steadily accumulating scientific evidence supports the general importance of oxidative damage of tissue and cellular components as a primary or secondary causative factor in many different human diseases and aging processes. Our goal has been to develop sensitive and reliable means to measure the oxidative damage and defense/repair status of an individual that could be easily used by a physician to determine whether there is an immediate or long-term increased health risk to their patients with regard to oxidative damage. We also sought to try to determine how this risk can best be reduced, and whether the prescribed therapy is working and how it might be best adjusted to optimize benefits. We have found that combining both an oxidative damage profile with a defense/repair profile produces the most reliable set of information to meet these objectives. Success is indicated by demonstrating the expected inverse correlation of oxidative stress vs. antioxidant status of a population of several hundred individuals. We also find support that oxidative stress status is under tight regulatory control for most individuals over a wide range of lifestyle variables including diet and exercise. Indeed only about 10% of the individuals analyzed appear to have unusually high oxidative stress levels. Only these individuals having the higher than normal levels of oxidative stress are the best responders to antioxidant supplements to lower their oxidative stress status to normal levels. We discuss the implications of these results for human application and review how current clinical studies are carried out to evaluate the benefits of antioxidant supplements in reducing the incidence of specific age-dependent disease. [ABSTRACT FROM AUTHOR]

Basic research suggests that oxidative stress may play an important role in many chronic diseases and provides plausible mechanisms by which natural antioxidants such as vitamin E may delay or prevent steps in atherogenesis. Dietary research has shown that those who consume higher amounts of fruits and vegetables have lower rates of heart disease and stroke, raising the possibility that antioxidants are protective. Results from large-scale human observational studies suggest that antioxidant consumption reduces the risk of developing cardiovascular disease (CVD). Both case-control and prospective cohort studies have carefully explored the relationship between vitamin E intake and plasma and tissue vitamin E levels and the risk of CVD. In many, but not all, of these studies vitamin E intake over an extended period was associated with decreased risk of cardiovascular events. Results from studies of blood levels are more limited and less consistent. This presentation summarizes data from the major observational studies. Overall, they support the possibility that vitamin E intake either from food or supplements may reduce risk of CVD; however, these studies have important limitations. For example, uncontrolled confounding can be similar in magnitude to the observed health effects, and antioxidant consumption may be merely a marker for a different cardioprotective factor (such as exercise or diet) that is responsible for these effects. In the search for small to moderate effects, randomized trials may be helpful, although to date, data from large-scale trials have been inconsistent. Several large-scale trials currently under way will help identify the potential benefits of vitamin E in the primary prevention of CVD and other chronic illness. Some are designed to test vitamin E alone as well as in combination with other antioxidant supplements because it is possible that antioxidants may be most effective if taken in particular combinations. Currently, the American Heart Association maintains that there are insufficient efficacy data from completed randomized trials to justify population-wide recommendations for use of vitamin E supplements in disease prevention. [ABSTRACT FROM AUTHOR]