Physiological Factors Predisposing to Neurotoxicity

Ray, David

doi:10.1007/978-3-642-60682-3_20

Cited by 8 publications

(2 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tobacco smoke is an important source of CO. Accordingly, the more a person smokes, the higher the carboxyhaemoglobin levels (Puente‐Maestu et al 1998), with known adverse effects on oxygen transportation by haemoglobin (McDonough & Moffatt 1999). However, the direct effects of smoke CO at a cellular level and its implication in diseases to related smoking remain to be completely elucidated.…”

mentioning

confidence: 99%

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

Alonso

Cardellach

López

et al. 2003

Pharmacology & Toxicology

214

113

View full text Add to dashboard Cite

Carbon monoxide (CO) toxicity is the result of a combination of tissue hypoxia and direct CO-mediated damage at a cellular level, since not all the signs and symptoms presented can be explained only by the formation of carboxyhaemoglobin. Mitochondria, specially the electron transport chain, seem to be the target for CO at a subcellular level. However, the direct effect of CO in individual complexes of the human mitochondrial respiratory chain has not been completely elucidated. We here studied the in vitro effect of CO on individual complexes of the mitochondrial respiratory chain of human mitochondria. We obtained muscle tissue from 10 healthy people who underwent orthopaedic surgery for hip replacement. Isolated mitochondria were incubated for 5 min. under CO concentrations of 50, 100 and 500 ppm. Afterwards, enzymatic activities of individual complexes of the mitochondrial respiratory chain were assessed in vitro and compared with those obtained in basal (synthetic air without CO) conditions. Cytochrome c oxidase (complex IV of the mitochondrial respiratory chain) activity showed a decrease from 836∫439 nmol/min

show abstract

mentioning

confidence: 99%

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

Alonso

Cardellach

López

et al. 2003

Pharmacology & Toxicology

214

113

View full text Add to dashboard Cite

show abstract

“…Noise exposure seems to play a role as well. 11 Hearing loss has been documented to occur because of the A1555G mutation without exposure to aminoglycosides. In 1 study, deafness was shown to occur with 50% penetrance by the age of 30 years and with 88% penetrance by the age of 65 years.…”

Section: The Mutationmentioning

confidence: 99%

Evaluating Pharmacogenetic Tests

Freund

Gregory²,

Clayton³

2004

Arch Pediatr Adolesc Med

View full text Add to dashboard Cite

Work in human genetics is revealing genes that affect the safe and effective use of pharmaceuticals. Primary care physicians are already receiving advertisements for tests for these variations that emphasize the value of learning about their patients' susceptibility to adverse reactions in order to avoid them. We propose a strategy for the critical evaluation of such offers to ensure the optimal use of these tests.

show abstract

Brain Morphogenesis and Developmental Neurotoxicology

Jensen

Olin

2018

Handbook of Developmental Neurotoxicology

View full text Add to dashboard Cite

Physiological Factors Predisposing to Neurotoxicity

Cited by 8 publications

References 26 publications

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

Carbon Monoxide Specifically Inhibits Cytochrome C Oxidase of Human Mitochondrial Respiratory Chain

Evaluating Pharmacogenetic Tests

Brain Morphogenesis and Developmental Neurotoxicology

Contact Info

Product

Resources

About