Fermín P. Pacheco-Moisés

Efficacy of Fish Oil on Serum of TNFα, IL-1β, and IL-6 Oxidative Stress Markers in Multiple Sclerosis Treated with Interferon Beta-1b

Multiple sclerosis (MS) is a chronic inflammatory disease, which leads to focal plaques of demyelination and tissue injury in the central nervous system. Oxidative stress is also thought to promote tissue damage in multiple sclerosis. Current research findings suggest that omega-3 polyunsaturated fatty acids (PUFAs) such as eicosapenta-enoic acid (EPA) and docosahexaenoic acid (DHA) contained in fish oil may have anti-inflammatory, antioxidant, and neuroprotective effects. The aim of the present work was to evaluate the efficacy of fish oil supplementation on serum proinflammatory cytokine levels, oxidative stress markers, and disease progression in MS. 50 patients with relapsing-remitting MS were enrolled. The experimental group received orally 4 g/day of fish oil for 12 months. The primary outcome was serum TNFα levels; secondary outcomes were IL-1β 1b, IL-6, nitric oxide catabolites, lipoperoxides, progression on the expanded disability status scale (EDSS), and annualized relapses rate (ARR). Fish oil treatment decreased the serum levels of TNFα, IL-1β, IL-6, and nitric oxide metabolites compared with placebo group (P ≤ 0.001). There was no significant difference in serum lipoperoxide levels during the study. No differences in EDSS and ARR were found. Conclusion. Fish oil supplementation is highly effective in reducing the levels of cytokines and nitric oxide catabolites in patients with relapsing-remitting MS.

INDICADORES DE ESTRÉS OXIDATIVO EN SUERO Y COMPORTAMIENTO ALIMENTARIO EN ADULTOS DE UNA ZONA RURAL DE JALISCO, MÉXICO

INTRODUCTION The feeding behavior establishes a relation of humans with food, includes food habits that could be involved with oxidative stress. OBJECTIVE To evaluate the relation of indicators of oxidative stress (lipid peroxides) and antioxidant (ascorbic acid, catalase, superoxide dismutase) with feeding behavior in adults of Teocuhitatlan Corona, Jalisco, Mexico. METHOD Study observational, descriptive, cross-sectional of 44 adults with 43 to 88 years, was used a instrument of feeding behavior. The questionnaire were related to indicators of oxidative stress. Were used descriptive statistics, frequency distribution and analysis of covariance with adjustment variables, was considered significant p <0.05. RESULTS The values of serum lipid peroxides were related to behaviors: consider the nutritional content as most important when choosing food (p = 0.042), dislike milk (p = 0.027), intake of sweets between meals (p = 0.001), habitual inclusion of vegetables and salads in main meal (p = 0.018). We do not found association in to values of ascorbic acid, cholesterol in low density lipoproteins and enzymatic activities of catalase and superoxide dismutase with food behaviors. DISCUSSION The feeding behaviors analyzed in this study may be involved with development of oxidative stress and could be have protective or harmful effect in development to complications of chronic non-communicable diseases and aging in this population. This suggests to analyze demographic and socio-cultural aspects of region and besides analyzing the consumption and metabolic markers related to food.

Alzheimer Disease and Metabolism: Role of Cholesterol and Membrane Fluidity

Alzheimers disease (AD) is an age-related disorder characterized by deposition of amyloid β-peptide (Aβ) and degeneration of neurons in brain regions such as the hippocampus, re‐ sulting in progressive cognitive dysfunction. The causes of Alzheimers disease (AD) have not been fully discovered, there are three main hypotheses to explain the phenomenon: a) The deficit of acetylcholine; b) The accumulation of beta-amyloid (Aβ and / or tau protein; and c) Metabolic disorders.

Oxidative Stress and Parkinson’s Disease: Effects on Environmental Toxicology

Epidemiological studies have found an increased risk of Parkinson’s disease (PD) with environmental factors such as exposure to substances derived from industrial processes, use of agrochemicals, or living in a rural environment. The hypothesis that certain environmental toxins could be the source of the EP is supported by the discovery that chemicals such as herbicides paraquat, diquat, and the fungicide maneb are selectively toxic in nigrostriatal dopaminergic neurons. Also, one of the insecticides produced by plants, such as rotenone, and by-product of the synthesis of synthetic heroin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) can be reproduced in animal models where neurochemicals, histopathological, and clinical characteristic of PD can be found. Interestingly, there are similarities in the chemical structure of paraquat and MPTP. Recent evidence exhibited that inflammation and oxidative stress play an essential role in the development of PD. So, in our laboratory we found that in an animal model melatonin decreases the products of lipid oxidation, nitric oxide metabolites, and the activity of cyclooxygenase 2, which are induced by an intraperitoneal injection of MPTP. This suggests that the neuroprotective effects of melatonin are partially attributed to its antioxidant scavenging and anti-inflammatory action.

Efficacy of Symbiotics in an Experimental Model of Endotoxic Shock Induced by Lipopolysaccharide from Escherichia Coli

Obsevation: Endotoxic shock is a life-threatening condition and its sequelae represent an array of clinical symptoms that encompass systemic inflammation, coagulopathy, and abnormalities of the renal, hepatic, pulmonary and hematologic systems, followed by multi-organ failure. Furthermore, systemic failure leads to an unfavorable environment in the gut that causes an imbalance in the homeostasis of intestinal microbiota. In the present study, the effect of symbiotics as adjuvant therapy in endotoxic shock was investigated. Adult male Wistar rats were randomized into three groups: Control group received a single intraperitoneal injection of physiological saline solution, and the other two groups received either a symbiotic formulation or a placebo daily, for one week, followed by the administration of a single lethal dose of lipopolysaccharide (LPS) from E. coli (20 mg/Kg, IP). Results: The symbiotic formulation used improved the survival rate of LPS-treated rats, ameliorated the clinical symptomatology, reduced the production of serum proinflammatory cytokines (TNF-α, IL-6, IL-1β), and preserved the mitochondrial membrane fluidity and ATPase activity. Conclusion: The symbiotic formulation used as a pre-treatment in this experimental model, reduced mortality and showed beneficial effects at the systemic and sub-cellular levels. *Corresponding author: Dr. Genaro Gabriel Ortiz, DevelopmentAging Laboratory, Neurodegenerative diseases, Division of Neurosciences, CIBO-IMSS, Sierra Mojada 800 CP 44340. Guadalajara, Jalisco, Mexico, Tel: (0133) 2015 3651; E-mail: genarogabriel@yahoo.com Received Date: April 13, 2016 Accepted Date: June 06, 2016 Published Date: June 09, 2016

Role of Mitochondria in Alzheimer ́s Disease

Alzheimers disease is the most common neurodegenerative disorder worldwide characterized by considerable atrophy and an enlargement and coarsening of the sulci, amyloid formation in neuritic plaques and brain vessels (amyloid angiopathy), neurofibrillary tangles, and neuronal loss, particularly in the limbic and association cortices. In addition, deficits in cholinergic transmission and associated loss of cholinergic cell bodies, granulovacuolar degeneration and rod-shaped eosinophilic inclusions (Hirano bodies) are common in Alzheimer’s disease patients. Clinical symptoms are characterized by progressive worsening of memory, and cognitive impairment accompanied by one of the following symptoms: aphasia, apraxia, agnosia and disorders in the executive function (Selkoe, 2004). The pathophysiological mechanisms that underlie the neurodegenerative characteristic of Alzheimers disease are yet to be completely understood, although many factors in disease pathogenesis have been identified, and several theories are emerged. In the last years, mitochondrial dysfunction has been considered as a potential factor implicated at some stage of the pathogenic process (Anandatheerthavarada et al., 2003; Sullivan & Brown, 2005;