scholarly journals Evidence that in vivo constriction of cerebral arterioles by local application of tert-butyl hydroperoxide is mediated by release of endogenous thromboxane.

Stroke ◽  
1987 ◽  
Vol 18 (1) ◽  
pp. 195-199 ◽  
Author(s):  
W I Rosenblum ◽  
D Bryan
2008 ◽  
Vol 46 (11) ◽  
pp. 3512-3521 ◽  
Author(s):  
Yong Pil Hwang ◽  
Jae Ho Choi ◽  
Eun Hee Han ◽  
Hyung Kyun Kim ◽  
Shin Keon Kang ◽  
...  

2002 ◽  
Vol 40 (5) ◽  
pp. 635-641 ◽  
Author(s):  
Chuen-Lan Liu ◽  
Jin-Ming Wang ◽  
Chia-Yih Chu ◽  
Ming-Tzong Cheng ◽  
Tsui-Hwa Tseng

2016 ◽  
pp. 617-626 ◽  
Author(s):  
M. KOHUTIAR ◽  
J. IVICA ◽  
R. VYTÁŠEK ◽  
A. SKOUMALOVÁ ◽  
J. ILLNER ◽  
...  

Isolated beef heart mitochondria have been exposed to tert-butyl hydroperoxide (tBHP) and peroxynitrite (PeN) in order to model the effects of reactive oxygen and nitrogen species on mitochondria in vivo. The formation of malondialdehyde (MDA), protein carbonyls, lipofuscin-like pigments (LFP), and nitrotyrosine was studied during incubations with various concentrations of oxidants for up to 24 h. The oxidants differed in their ability to oxidize particular substrates. Fatty acids were more sensitive to the low concentrations of tBHP, whereas higher concentrations of PeN consumed MDA. Oxidation of proteins producing carbonyls had different kinetics and also a probable mechanism with tBHP or PeN. Diverse proteins were affected by tBHP or PeN. In both cases, prolonged incubation led to the appearance of proteins with molecular weights lower than 29 kDa bearing carbonyl groups that might have been caused by protein fragmentation. PeN induced nitration of protein tyrosines that was more intensive in the soluble proteins than in the insoluble ones. LFP, the end products of lipid peroxidation, were formed more readily by PeN. On the other hand, fluorometric and chromatographic techniques have confirmed destruction of LFP by higher PeN concentrations. This is a unique feature that has not been described so far for any oxidant.


2010 ◽  
Vol 119 (2) ◽  
pp. 580-585 ◽  
Author(s):  
Pin-Der Duh ◽  
Bor-Sen Wang ◽  
Shiou-Jen Liou ◽  
Chia-Jung Lin

2012 ◽  
Vol 133 (2) ◽  
pp. 337-343 ◽  
Author(s):  
Sung-Yong Yang ◽  
Chung-oui Hong ◽  
Hojoung Lee ◽  
Sang-yul Park ◽  
Byung-gyu Park ◽  
...  

2004 ◽  
Vol 94 (2-3) ◽  
pp. 345-351 ◽  
Author(s):  
Patrícia Valentão ◽  
Márcia Carvalho ◽  
Félix Carvalho ◽  
Eduarda Fernandes ◽  
Ricardo Pires das Neves ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Wenxian Zhou ◽  
Yifeng Shi ◽  
Hui Wang ◽  
Caiyu Yu ◽  
Huanqing Zhu ◽  
...  

As a common degenerative disease, osteoarthritis (OA) usually causes disability in the elderly and socioeconomic burden. Previous studies have shown that proper autophagy has a protective effect on OA. Sinensetin (Sin) is a methylated flavonoid derived from citrus fruits. Studies have shown that Sin is a good autophagy inducer and has shown excellent therapeutic effects in a variety of diseases; however, its role in the treatment of OA is not fully understood. This study proved the protective effect of Sin on OA through a series of in vivo and in vitro experiments. In vitro experiments have shown that Sin may inhibit chondrocyte apoptosis induced by tert-butyl hydroperoxide (TBHP); at the same time, it might also inhibit the production of MMP13 and promote the production of aggrecan and collagen II. Mechanism studies have shown that Sin promotes chondrocyte autophagy by activating AMPK/mTOR signaling pathway. On the contrary, inhibition of autophagy can partially abolish the protective effect of Sin on TBHP-treated chondrocytes. In vivo experiments show that Sin may protect against DMM-induced OA pathogenesis. These results provide evidence that Sin serves as a potential candidate for the treatment of OA.


1990 ◽  
Vol 80 (2) ◽  
pp. 226-232
Author(s):  
Tomoaki Matsuo ◽  
Yumiko Kashiwaki ◽  
Saburo Itoo

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