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Jha M.N.,Ecosystems Protection Program | Bedford J.S.,Colorado State University | Jha S.,North Shore Medical Center | Prasad K.N.,Premier Micronutrient Corporation
International Journal of Low Radiation | Year: 2011

We investigated the effect of caffeine on low dose γ-radiation- induced chromosomal damage in human T-cell leukaemia cells (Jurkat T-cells) and two normal human fibroblast cell lines (AG1522 and GM2149). Low doses of gamma-radiation were found to increase the levels of chromatid gaps and breaks in a dose-dependent manner in both normal and cancer cells; however, cancer cells appeared to be more sensitive than the normal cells. Caffeine treatment before radiation exposure significantly increased the levels of chromatid gaps and breaks in Jurkat T-cells at all radiation doses, but it did not increase the level of these aberrations in normal cells. The mechanisms of this differential effect of caffeine in cancer cells and normal cells are unknown; however, G2-delay allows more time for rejoining of chromosome breakage to occur, then elimination of this delay by caffeine in tumour cells, not in normal cells might account for difference. Copyright © 2011 Inderscience Enterprises Ltd.

Prasad K.N.,Premier Micronutrient Corporation | Bondy S.C.,University of California at Irvine
Brain Research | Year: 2015

Post-traumatic stress disorder (PTSD) is a complex mental disorder with psychological and emotional components, caused by exposure to single or repeated extreme traumatic events found in war, terrorist attacks, natural or man-caused disasters, and by violent personal assaults and accidents. Mild traumatic brain injury (TBI) occurs when the brain is violently rocked back and forth within the skull following a blow to the head or neck as in contact sports, or when in close proximity to a blast pressure wave following detonation of explosives in the battlefield. Penetrating TBI occurs when an object penetrates the skull and damages the brain, and is caused by vehicle crashes, gunshot wound to the head, and exposure to solid fragments in the proximity of explosions, and other combat-related head injuries. Despite clinical studies and improved understanding of the mechanisms of cellular damage, prevention and treatment strategies for patients with PTSD and TBI remain unsatisfactory. To develop an improved plan for treating and impeding progression of PTSD and TBI, it is important to identify underlying biochemical changes that may play key role in the initiation and progression of these disorders. This review identifies three common biochemical events, namely oxidative stress, chronic inflammation and excitotoxicity that participate in the initiation and progression of these conditions. While these features are separately discussed, in many instances, they overlap. This review also addresses the goal of developing novel treatments and drug regimens, aimed at combating this triad of events common to, and underlying, injury to the brain. © 2014 Elsevier B.V.

Prasad K.N.,Premier Micronutrient Corporation
NATO Science for Peace and Security Series A: Chemistry and Biology | Year: 2013

There are two types of radiological weapon, "dirty bomb," and nuclear weapon (atom bomb). A dirty bomb can be made from one or more commercially available radioactive isotopes and it can be detonated using a conventional explosive, whereas an atom bomb consists of fissionable element, and it requires complex procedures for detonation. Explosion of a radiological weapon can cause a few injuries to mass casualties, depending upon the type of radiological weapon, and can increase the chronic health risks among survivors. Bio-Shield refers to chemicals or biologics that can prevent or mitigate radiation injury when administered before and/or after irradiation. During past decades, several radiation preventive and mitigating agents been identified. They can be grouped into following categories: (a) chemicals not approved by the FDA, (b) drugs approved by the FDA for other conditions, (c) certain biologics approved by the FDA, and (d) antioxidants and herbs not requiring FDA approval. An effective bio-shield that can be recommended to humans must satisfy the following three criteria: (1) chemicals or biologics should prevent and/or mitigate radiation damage in the laboratory experiments when administered before and/or after irradiation; (2) they should show at least some evidence that they can prevent or mitigate radiation damage in humans; and (3) they at radiation preventive or radiation mitigating doses must be safe in human when administered on a short- or long-term basis. Published data show that most radiation preventing and mitigating chemicals, drugs or herbs satisfy only the first criterion of an effective bio-shield, whereas antioxidants satisfy all three. © 2013 Springer Science+Business Media Dordrecht.

Prasad K.N.,Premier Micronutrient Corporation | Bondy S.C.,University of California at Irvine
Current Aging Science | Year: 2014

A link between Alzheimer's disease (AD) and an excess presence of oxidant free radicals in the brain has frequently been reported. It is generally assumed that such oxidative stress and related cellular damage is caused by inflammatory changes in the brain and is consequent to amyloid deposition. This review makes the argument that elevated oxidative stress in AD is an early causal event in the initiation and advancement of this disease. Oxidative stress can be decreased by enhancing antioxidant enzymes through activation of the cytoplasmic transcriptional factor (Nrf2)/ARE (antioxidant response element) pathway, and by dietary and endogenous antioxidant chemicals. Reduction in the binding ability of Nrf2 to ARE lowers antioxidant enzyme levels. Decreased levels of Nrf2 and augmentation of oxidative stress in AD suggest that the ROS-dependent mechanism of activating the Nrf2/ARE pathway has become unresponsive. A combination of agents that can either activate the Nrf2-ARE pathway by ROS-independent mechanisms, or by acting directly as antioxidant chemicals, may be necessary to reduce oxidative stress in AD. Earlier shortcomings of using individual antioxidants may be due to consideration of antioxidants as pharmacological agents, ignoring the fact that individual antioxidants can be transmuted in the highly oxidant milieu that is present in AD. Interactions between various cellular compartments may require simultaneous examination of more than one agent. The clinical utility of such a more integrative method can reveal interactive effects such as those found in nutritional research and this can compensate for any mechanistic shortcomings of simultaneous testing of more than a single agent. © 2014 Bentham Science Publishers.

Prasad K.N.,Premier Micronutrient Corporation | Bondy S.C.,University of California at Irvine
Current Aging Science | Year: 2013

Recently the relationship between oxidative stress and aging has been brought into question. It has been suggested that while oxidative events may play a role in the progression of age-related pathologies, it is not relevant to aging processes not involving specific diseases associated with senescence. The evidence in support of this concept is largely based on studies with the roundworm, Caenorhabditis elegans (C. elegans) that has been extensively used as a model system to study aging. This commentary evaluates data derived from C. elegans and documents that the preponderance of evidence from this species supports the role of pro-oxidant events as being a significant contributor to normal aging. Possible reasons for some anomalous findings conflicting with this concept, are discussed. © 2013 Bentham Science Publishers.

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