Genotoxicity of chloroquine in rat liver cells: Protective role of free radical scavengers

2006 ◽  
Vol 22 (3) ◽  
pp. 159-167 ◽  
Author(s):  
E. O. Farombi
Toxicology ◽  
2011 ◽  
Vol 289 (2-3) ◽  
pp. 175-184 ◽  
Author(s):  
Irene Antolino-Lobo ◽  
Jan Meulenbelt ◽  
Jeffrey Molendijk ◽  
Sandra M. Nijmeijer ◽  
Peter Scherpenisse ◽  
...  

1983 ◽  
Vol 245 (1) ◽  
pp. H139-H142 ◽  
Author(s):  
W. I. Rosenblum

Mouse pial arterioles were exposed to the free radical-generating reactants acetaldehyde and xanthine oxidase. Concentrations of 0.5 mM acetaldehyde and 0.1 U/ml xanthine oxidase caused reversible dilations, whereas higher concentrations produced initial constrictions followed by reversible dilations. The following free radical scavengers inhibited the dilation when added to the lower concentrations of reactants: superoxide dismutase, a superoxide scavenger; catalase, an H2O2 scavenger; and mannitol, a hydroxyl scavenger. In addition, pretreatment of the animal with dimethyl sulfoxide, a hydroxyl scavenger, also inhibited the response. The scavengers were also tested against either the dilation produced by increased inspired CO2 or against the dilation produced by local application of 10(-3) M papaverine. No significant effect was observed. The data support the hypothesis that hydroxyl radicals can dilate pial arterioles, since all the scavengers can ultimately reduce levels of hydroxyl generated by acetaldehyde plus xanthine oxidase.


1984 ◽  
Vol 223 (3) ◽  
pp. 879-883 ◽  
Author(s):  
L A Videla ◽  
M I Villena ◽  
G Donoso ◽  
C Giulivi ◽  
A Boveris

The addition of t-butyl hydroperoxide to perfused rat liver elicited a biphasic effect on hepatic respiration. A rapid fall in liver oxygen consumption was initially observed, followed by a recovery phase leading to respiratory rates higher than the initial steady-state values of oxygen uptake. This overshoot in hepatic oxygen uptake was abolished by free-radical scavengers such as (+)-cyanidanol-3 or butylated hydroxyanisole at concentrations that did not alter mitochondrial respiration. (+)-Cyanidanol-3 was also able to facilitate the recovery of respiration, the diminution in the calculated rate of hydroperoxide utilization and the decrease in liver GSH content produced by two consecutive pulses of t-butyl hydroperoxide. It is suggested that the t-butyl hydroperoxide-induced overshoot in liver respiration is related to increased utilization of oxygen for lipid peroxidation as a consequence of free radicals produced in the scission of the hydroperoxide by cellular haemoproteins.


2011 ◽  
Vol 43 (04) ◽  
pp. 268-274 ◽  
Author(s):  
M. Leyendecker ◽  
P. Korsten ◽  
R. Reinehr ◽  
B. Speckmann ◽  
D. Schmoll ◽  
...  

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