Logo

Garden City
Plainview
Listen to The Optimal Health Program for latest on Stem Cell Therapy Treatments on WOR radio (710 on the AM dial) on Saturday mornings from 7-8 AM and WABC Radio 770 A.M. Sunday evenings from 10-11PM
Click Here for Telemedicine Consultation & Appointment

Daily Archives for: May 19th, 2008

Recently, decreased glutamate (Glu) and reduced glutathione (GSH) levels were reported in the quadriceps femoris of patients with chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate whether Glu and GSH levels are also modified in the diaphragm of these patients. Nine male COPD patients (forced expiratory volume in one second (FEV1) range 28-68% of the predicted value) and seven male patients with normal pulmonary function (mean SD FEV1 86 3% pred) submitted to thoracotomy were included.

In smoking subjects with obvious emphysema, the interaction between neutrophil-derived MPO and H2O2 produced by alveolar inflammatory cells (alveolar macrophages (AM) and polymorphonuclear neutrophils (PMN)) has the ability to spontaneously inactivate, in vitro, the alpha 1 proteinase inhibitor (alpha 1PI). This inactivation can induce a desequilibrium of the protease-antiprotease balance in the lungs. In this study,

Glutathione (GSH), a ubiquitous tripeptide thiol, is a vital intra- and extracellular protective antioxidant in the lungs. The rate-limiting enzyme in GSH synthesis is g-glutamylcysteine synthetase (g-GCS). The promoter (58-flanking) region of the human g-GCS heavy and light subunits are regulated by activator protein-1 and antioxidant response elements. Both GSH and g-GCS expression are modulated by oxidants,

Inflammatory lung diseases are characterized by chronic inflammation and oxidant/antioxidant imbalance, a major cause of cell damage. The development of an oxidant/antioxidant imbalance in lung inflammation may activate redox-sensitive transcription factors such as nuclear factor-kB, and activator protein-1 (AP-1), which regulate the genes for pro-inflammatory mediators and protective antioxidant genes. Glutathione (GSH), a ubiquitous tripeptide thiol,

Catechins, polyphenolic compounds belonging to flavanoid family, have been reported to posses insulin-like properties and their antidiabetic actions have also been documented. Recently catechins have received much attention as strong anti-oxidative agents. Since oxidative stress has been implicated in the development of diabetic complications and GSH plays an important role in portection against oxidative damages,

Blood samples were analyzed for GSH and GSH redox state in 40 age-related macular degeneration (ARMD) patients (> 60 y), 33 non-ARMD diabetic patients (> 60 years), 27 similarly aged non-ARMD and nondiabetic individuals (> 60 years), and 19 younger individuals (< 60 years) without ARMD or diabetes. Results showed a significantly lower plasma GSH in older individuals (ARMD,

To evaluate the relationship between oxidative stress and glucose metabolism, insulin sensitivity and intraerythrocytic reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio were measured in 10 non- insulin-dependent diabetes mellitus (NIDDM) patients and 10 healthy subjects before and after the intravenous administration of GSH. In particular, after baseline insulin sensitivity was assessed by a 2-hour euglycemic hyperinsulinemic clamp,

Objective: Hyperglycemia is considered a primary cause of diabetic vascular complications and is associated with oxidative stress, impaired trace element and lipid metabolism as well as pancreatic enzyme abnormalities. The role of trace elements in some of the metabolic dysfunctions and their contributions in the development of vascular complications is not clear. Therefore,

Oxidative stress has been proposed as a possible pathogenic factor for diabetic complications. It is relevant in determining cell replicative capacity and life span, and in vitro antioxidant results is able to reverse the impaired proliferative activity of different cell types. It was recently demonstrated that cultured skin fibroblasts from insulin-dependent diabetic patients with nephropathy age prematurely and have a shorter life cell cycle.

The destructive pathologic and biochemical consequences of methyl mercury have been extensively described. Relatively little is known, however, about the defensive mechanisms neurons employ to protect themselves against mercurial injury. Studies using a variety of cell types have disclosed several inducible biochemical responses to heavy metal and pro-oxidant insult. These responses include modulation of cellular levels of glutathione,