High impact information on o-Biphenylamine

• Inhibition of Ca2+ signaling by 2-aminobiphenyl borate blocked Ang II-dependent COX-2 expression [1].
• 4-Aminobiphenyl (4-ABP) and its analogue, 2-aminobiphenyl (2-ABP), were examined for their ability to induce oxidative DNA damage in Hep G2 cells [2].
• The remaining two chemicals would have been missed in the absence of a mouse bioassay (2-aminobiphenyl (2185-92-4) and captan (133-06-2)) and thus are good candidates for evaluation in the short term bioassays in transgenic mice currently being validated [3].
• A concentration-dependent increase in the generation of the superoxide anion radical (O-2), was observed during the incubation of benzidine (0.1-5 mM), but not of the structurally related compounds 4-aminobiphenyl, 2-aminobiphenyl or 4-fluoro-4'-aminobiphenyl, with NADPH-supplemented rat liver microsomes [4].
• It was found that samples of urine collected for 24 h after the administration of the carcinogens, benzidine, 4-aminobiphenyl and 2-aminonaphthalene, showed significantly mutagenic activity, whereas no mutagenicity was observed in urine after treatment with 3,3'-5,5'-tetramethylbenzidine, 2-aminobiphenyl and 1-aminonaphthalene [5].

Associations of o-Biphenylamine with other chemical compounds

• Carcinogenesis bioassay in rats and mice fed diets containing 2-biphenylamine hydrochloride [6].

Gene context of o-Biphenylamine

• EGF did not induce Ca2+ mobilization, and 2-aminobiphenyl borate did not inhibit EGF-dependent COX-2 expression [1].

Analytical, diagnostic and therapeutic context of o-Biphenylamine

• HPLC and TLC analytical techniques were used for separation and detection of [14C] 2-aminobiphenyl and its metabolites [7].

References