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1 cells treated with the antioxidant butylated hydroxyanisole.
2 ntioxidant standards quercetin and butylated hydroxyanisole.
3 mopreventive agents ethoxyquin and butylated hydroxyanisole.
4 oxygen species and was blocked by butylated hydroxyanisole.
7 ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the lu
8 the antioxidants N-acetylcysteine, butylated hydroxyanisole, and pyrrolidine dithiocarbamate and was
10 was very high, similar to that of butylated hydroxyanisole (BHA) and higher than that of other synth
11 Inhibition of ATO-induced ROS with butylated hydroxyanisole (BHA) does not affect Nrf2 activation or
12 Administration of 0.75% 2(3)-tert-butyl-4-hydroxyanisole (BHA) in AIN-76A diet to female CD-1 mice
16 iet that contained the antioxidant butylated hydroxyanisole (BHA), and others were given daily intrap
17 e synthetic phenolic antioxidants, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and
19 rolidinedithiocarbamate (PDTC) and butylated hydroxyanisole (BHA), indicating that the generation of
20 ocopherol, catechin, lycopene, and butylated hydroxyanisole (BHA)] for conjugated dienes (during a 90
21 -2 (Nrf2) activators (oltipraz and butylated hydroxyanisole) can induce hepatic Mrp transporters and
22 d Nrf2-null mice with oltipraz and butylated hydroxyanisole demonstrated that the induction of Mrp2,
23 e of cell death, the ROS scavenger butylated hydroxyanisole efficiently blocked TNF-induced necrotic
25 tructurally unrelated antioxidants butylated hydroxyanisole, N-acetyl-L-cysteine, and pyrrolidine dit
26 of CHO cells with the antioxidants butylated hydroxyanisole or butylated hydroxytoluene blocked the t
27 tioxidants N-acetyl-l-cysteine and butylated hydroxyanisole, or an inhibitor of NADPH oxidase, diphen
28 ncluding butylated hydroxytoluene, butylated hydroxyanisole, TEMPOL (4-hydroxy-2,2,6, 6-tetramethylpi
29 a pancaspase inhibitor but not by butylated hydroxyanisole, which inhibits reactive oxygen species.
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