The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

A convenient approach for evaluating the toxicity profiles of in vitro neuroprotective alkylaminophenol derivatives.

The cytotoxicity profiles of a series of quinol-type derivatives were examined through simple Escherichia coli plate assays discriminating the two main cytotoxicity mechanisms associated with polyphenol oxidation to quinone. Toxicity mediated by reactive oxygen species ( ROS- TOX) was detected in the OxyR(-) assay using cells sensitive to oxidative stress due to a deficiency in the OxyR function. Toxicity arising from the high susceptibility of quinone toward endogenous nucleophiles (Q-TOX) was detected using OxyR(+) cells, in the presence of a nitric oxide donor to promote the quinol oxidation to the corresponding quinone. The toxicity profile markedly depended on structural features. Strong ROS- TOX required a pyrogallol arrangement (exifone; 2,3,4-trihydroxybenzophenone, 1; baicalein) or a 2-aminoresorcinol sequence (3-amino-2,4-dihydroxybenzophenone, 4). The pyrogallol moiety determined a low Q-TOX, suggesting the conversion of quinones into oxidation products of low toxicity. Compounds lacking a 2-hydroxyl substituent (derivatives 2 and 5, related to 1 and 4, respectively) induced a weak ROS- TOX, but a significant Q-TOX. The electrochemical oxidation of the studied compounds corroborated the crucial role of the 2-hydroxyl group, which had two effects: to protect the quinonoid species from Michael addition, the reaction at the origin of Q-TOX, and, due to the contraction of hydrogen bonding, to stabilize every intermediary oxidation product, very likely involved in ROS- TOX.[1]


  1. A convenient approach for evaluating the toxicity profiles of in vitro neuroprotective alkylaminophenol derivatives. Urios, A., Largeron, M., Fleury, M.B., Blanco, M. Free Radic. Biol. Med. (2006) [Pubmed]
WikiGenes - Universities