Chemical incompatibilities can lead to a decrease in drug delivery, drug degradation, and/or production of toxic products.
Furthermore, varying levels of b5 function important for drug oxidation can also produce altered metabolite ratios, potentially increasing the production of toxic products in certain instances.
One major focus was the development of chemical reactions that reduced or eliminated the use of toxic substances and the production of toxic by-products.
Encephalopathy is actually caused by the production of toxic side products like acetaldehyde and chloral hydrate [25, 26].
A larger production of toxic oxygenated products was observed with increasing pressures, while low pressures promoted the formation of soot precursors.
The sustained or elevated toxicity was likely associated with the production of toxic intermediates (see Table S1 of the Supporting Information and a detailed discussion below).
Granulocyte colony-stimulating factor, by augmenting white cell production, pulmonary sequestration and margination and production of toxic oxygen species, may exacerbate underlying subclinical bleomycin pulmonary toxicity.
Some physiologists suggest that this pathway is a mechanism to prevent overreduction of the respiratory pathway, which would lead to the production of toxic free radicals.
Dysfunction of the respiratory chain leads to decreased energy production and to an increase in the production of toxic reactive oxygen species.
Treatment with 2- 2-nitro-4-trifluoromethylbenzoyl -1,3-cyclohexanedione (NTBC), a potent inhibitor of the tyrosine catabolic pathway, prevents the production of toxic metabolites.
Alzheimer's researchers and drug companies have for years concentrated on one hallmark of Alzheimer's disease: the production of toxic shards of a protein that accumulate in plaques on the brain.
