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Biomedical subjects

D Romero-Alvira

Publications and source records attributed to D Romero-Alvira.

7 recordsLinked to original sources

The keys of oxidative stress in acquired immune deficiency syndrome apoptosis.

Apoptosis is the main cause of CD4+ T-lymphocyte depletion in acquired immune deficiency syndrome (AIDS). Various agents appear to be able to trigger apoptosis in CD4+ T cells, including viral proteins (i.e. gp120, Tat), inappropriate secretion of inflammatory cytokines by activated macrophages (i.e. tumor necrosis factor alpha) and toxins produced by opportunistic micro-organisms. Since oxidative stress can also induce apoptosis, it can be hypothesized that such a mechanism could participate in CD4+ T-cell apoptosis observed in AIDS. This correlates strongly with the observation that AIDS patients present low levels of antioxidants (i.e. superoxide dismutase-Mn, vitamin E, selenium and glutathion) most likely due to inappropriate nutrition (i.e. diets poor in antioxidants), alcohol and drug consumption, and digestive problems associated with the disease. Furthermore, the coadministration of the antiviral drug zidovudine with antioxidants increases its therapeutic potential. Finally, the following additional observations support the hypothesis that oxidative stress is involved in cell apoptosis in AIDS: (1) The depletion of the anti-apoptotic/antioxidant protein Bcl-2 in human immunodeficiency virus (HIV)-infected CD4+ cells; (2) a decrease of apoptosis in HIV-infected cells treated with antioxidants and; (3) the presence of the pro-apoptotic/pro-oxidant cytokines secreted by activated macrophages in AIDS patients. Therefore, anti-apoptotic/antioxidant strategies should be considered, alongside antiviral strategies, in order to design a more efficient therapy for AIDS in the near future.

Acquired Immunodeficiency Syndrome↗

High blood pressure, oxygen radicals and antioxidants: etiological relationships.

This hypothesis proposes that high blood pressure is a pathological state associated with a loss of the balance between pro-oxidation and antioxidation, energy depletion, and accelerated aging in the target organs, such as heart, kidney and brain. Different nutritional, environmental, pharmacological factors and/or associated pathologies (diabetes, arteriosclerosis, cancer, alcoholism, etc.) and/or genetic components, can induce high blood pressure by breaking the redox equilibrium in the affected organs. Additional evidence, such as increase of oxidative damage, fibrogenesis, inhibition of the cardiocytic sodium-potassium pump, and heart hypertrophy, supports this hypothesis. These facts are analysed in the present paper, showing that they could contribute to the development of high blood pressure and associated pathologies by oxidative mechanisms.

Animals↗

Cardiomyopathies and oxidative stress.

Cardiomyopathies are the group of diseases affecting the cardiac muscle. Although they have never been related to oxidative stress diseases, an analysis of the causes of these pathologies reveals the presence of a pro-oxidative agent or that the intracardiocytic balance between oxidation and antioxidation has been broken. In support of this hypothesis, we analyse the pro-oxidative factors which co-operate with other factors or by themselves to promote the development of this group of pathologies. We show also data demonstrating that the tissue and cellular damages are characteristic of an oxidative stress situation. Finally, we present evidence that in some cases of particular cardiomyopathies, the use of antioxidative strategies greatly improves the health of the patients. Therefore, we suggest that the use of antioxidants can be an alternative or complementary therapy in this group of diseases.

Alcoholism↗

Role of oxygen free radicals in altitude-related disorders.

A massive expansion of mountain tourism and the practice of sports at altitude (mountaineering, skiing, cycling, hang-gliding, parapente, etc) has been observed in the last decades. This emphasis on new forms of sports and recreation represented as a social phenomenon is accompanied by an increase in the mountain associated-disorders and related-accidents. These include headache, lassitude, pain, difficulty in breathing, rapid heartbeat, and in the worst of the cases loss of consciousness, always possible, manifest by poor judgement, fatigue, etc, and death. However, medical studies are rare, mainly because the molecular mechanisms of tissue damage induced by oxygen free radicals are still poorly understood. Therefore, the goals of the present report are: 1) to summarize the main adaptations of the body at high altitude, introducing the concepts of altitude sickness and oxygen free radicals and their relation; 2) to propose a mechanism of action of oxygen free radicals in the development of this pathology, with special attention in hypoxia and related mechanisms; 3) to suggest a role for antioxidants in the therapy of altitude-related disorders.

Acclimatization↗

Oxidative stress in some dementia types.

By analogy to some pathologies (such as demyelinating diseases, arthritis and inflammatory processes) where the loss of cellular integrity is the starting point of tissue oxidative damage, it is proposed that some dementia types could be derived from a similar mechanism. The following oxidative events are proposed: (a) different agents could alter capillary or neuron integrity with the subsequent leakage of oxidases, proteases and transition metals from cellular compartments; (b) the persistence of the damaging agent, possible depletion of antioxidative defenses and concomitant loss of neuron function; (c) alteration of adjacent cells in the same manner; and (d) finally localized brain necrosis and progression of the dementia.

Alzheimer Disease↗