2 3 dihydroxybenzoic acid/hypoxia

Carbon monoxide poisoning produces both immediate and delayed neuronal injury in selective regions of the brain that is not readily explained on the basis of tissue hypoxia. One possibility is that cellular injury during and after CO poisoning is related to the production of reactive oxygen species

HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the

Increasing the blood's capacity for oxygen transport by erythropoiesis-stimulating agents (ESAs) constitutes a prohibited procedure of performance enhancement according to the World Anti-Doping Agency (WADA). The advent of orally bio-available small-molecule ESAs such as hypoxia-inducible factor

This study was to investigate the effects of bradykinin (BK) on myocyte cultures. The effects of BK against lipid peroxidation and oxygen free radicals were estimated on an anoxia/reoxygenation injured model. A salicylate hydroxylation product dihydroxybenzoic acids (DHBA) was detected using HPLC

OBJECTIVE The primary goal of this study was to test whether high-altitude exposure (HAE: 0.9% O(2) at 0.47 ATA for 24 hours) was capable of increasing the systemic inflammatory markers as well as the toxic organ injury indicators in rats, with a secondary goal to test whether preinduction of heat

To study the involvement of oxidative stress in 6-OHDA neurotoxicity, we investigated the production of the hydroxyl free radical (OH.) in the substantia nigra (SN) and the striatum (CS) several moments after intranigral injection of the neurotoxin, with or without an added episode of hypoxia (30

Neurotrophins are critical for the survival of neurons during development and insufficient access to neurotrophins later in life may contribute to the loss of neurons in neurodegenerative disease, spinal cord injury, and stroke. The prolyl hydroxylase inhibitors ethyl 3,4-dihydroxybenzoic acid (DHB)

OBJECTIVE To study the effect of melatonin on the production of hydroxyl radical (.OH) and lactate dehydrogenase (LDH) following hypoxia in cortical slice. METHODS Cortical slice was incubated with artificial cerebrospinal fluid (ACSF) in tube. Hypoxia was achieved by substituting 91.6% N2 and 8.4%

Isolated rat brain microvessels have been utilized to examine whether they produce hydroxyl free radicals if they are subjected to a 10- to 20-min anoxia period followed by a 40-min reoxygenation period. Hydroxyl free radical flux was assessed utilizing salicylate as a trap. The 2,3- and

Oxygen-sensing prolyl-hydroxylase (PHD)-2 negatively regulates hypoxia-inducible factor (HIF)1-α and suppresses the hypoxic response. Hypoxia signaling is thought to be proinflammatory but also attenuates cellular injury and apoptosis. Although increased hypoxic response has been noted in asthma,

Hypoxia-ischemia with reperfusion is known to cause reactive oxygen species-related damage in mammalian systems, yet, the anoxia tolerant freshwater turtle is able to survive repeated bouts of anoxia/reoxygenation without apparent damage. Although the physiology of anoxia tolerance has been much

To better understand the mechanisms of tissue injury during and after carbon monoxide (CO) hypoxia, we studied the generation of partially reduced oxygen species (PROS) in the brains of rats subjected to 1% CO for 30 min, and then reoxygenated on air for 0-180 min. By determining H2O2-dependent

Reactive oxygen species (ROS) have been implicated in the pathogenesis of neuronal injury after carbon monoxide (CO) poisoning. Severe CO poisoning is treated with hyperbaric oxygen (HBO), which eliminates CO quickly from hemoglobin and body tissue stores, but has a potential to increase ROS

We hypothesized that selective brain hypothermia (SBHT) decreases production of hydroxyl radicals (*OH) induced by hypoxia-ischemia (H-I) and reperfusion and attenuates neuronal damage in neonatal rat brain. Anesthetized 7-day-old rats were divided into a normothermia (NT) group (n=6) and a SBHT

The difficulty in direct detection of oxygen-derived free radicals (OFR) in the intact kidney has left uncertain the role of OFR in renal hypoperfusion injury. Salicylate hydroxylation was used as a sensitive method of estimating the extent of production of highly reactive hydroxyl radicals in renal