Homeostatic regulation of the endoneurial microenvironment during development, aging and in response to trauma, disease and toxic insult

ABSTRACT Oxidative DNA damage is an inevitable consequence of cellular metabolism, with a propensity for increased levels following toxic insult. Although more than 20 base lesions have been identified, only a fraction of these have received appreciable study, most notably 8-oxo-2�deoxyguanosine

an ou t skin is a major target for toxic insult by a broad spectrum regulation pathways, and alterations in the differentiation, Chompoo et al. BMC Complementary and Alternative Medicine 2012, 12:106

Mammalian cells have evolved numerous complicated mechanisms that protect against toxic insults. Phase II en-zymes are the primary lines of defense against reactive chem-ical species generated by exogenous quinines and related

-cological challenges may reveal or unmask deficits that may not be evident under basal testing conditions. The purpose of this chapter is to discuss how assessment of pharmacological and stress vulnerability has proved to be useful in revealing alterations in offspring exposed to developmental toxicants. Studies

has on the liver enzymes [aspartate aminotransferase (SGOT), alanine aminotranferease (SGPT), alkaline phosphatase (ALP), and gamma-glutamyltrans-ferase (GGT)] of rats under this toxic insult. Male rats in groups (A, B, C and D) were intraperitoneally injected with different sub-lethal increasing

induced in wild-type and p38β knockout neu-rons was not significantly different. In contrast, selective inhibition of neuronal p38α was neuroprotective. Our results show that neuronal p38β is not required for neurotoxicity induced by multiple toxic insults, but that p38α in the neuron contributes

proteins, signal transduction, and solute transporters. Seven differentially expressed transcripts were confirmed by real-time quantitative polymerase chain reaction. In addition, significantly increased peroxide levels support the implication of oxidative stress in UN toxicant response. This report

proper development. A related problem is the redundancy of compensatory systems in the brain. Such systems may disguise the severity of the initial toxic insult and themselves can cause functional disturbances. To study neuronal development in a system that minimizes such difficulties, we have grafted

be observed through some biochemical parameters. Impairment of the liver generally occurs from excessive exposure to xenobiotics, alcohol, chemotherapeutic agents, virus and protozoan infections. Depending upon the severity of toxicant insult, hepatic cell injury can lead from acute to chronic hepatitis