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Studies on Ni(II)-induced carcinogenesis have suggested that oxidative damage caused by Ni(II) may in part be due to increased tissue H2O2 formation. However, there is lack of evidence in vivo. Because of limitations of available methods for direct measurement of the in vivo rate of H2O2 formation in animals, Ni(II)-induced production of H2O2 was estimated from changes in the rate of glutathione disulfide (GSSG) formation. Male B6C3F1 mice (6-8 wk old) were injected i.p. with 170 mumol NiAc2/kg. Biliary efflux and liver, kidney, and lung levels of glutathione (GSH and GSSG) were determined 0-2 h after treatment. In spite of slight increases in tissue GSSG levels by Ni(II), there was no significant change in the biliary efflux of GSSG. Pretreatment with 50 mg/kg (i.p.) of bis-chloroethyl-nitrosourea (BCNU), an inhibitor of GSSG reductase, did not augment the effects of Ni(II) on GSSG formation significantly. Based on these observations, it was apparent that Ni(II) did not change the concentration of H2O2 significantly in vivo.
J Chang, and
H Jaeschke, and
K Randerath
January 1989,
Chemico-biological interactions,
J Chang, and
H Jaeschke, and
K Randerath
June 2001,
Journal of neurochemistry,
J Chang, and
H Jaeschke, and
K Randerath
January 1977,
Medycyna pracy,
J Chang, and
H Jaeschke, and
K Randerath
June 2022,
Medical archives (Sarajevo, Bosnia and Herzegovina),
J Chang, and
H Jaeschke, and
K Randerath
January 1975,
Annals of the New York Academy of Sciences,
J Chang, and
H Jaeschke, and
K Randerath
November 1990,
Archives of biochemistry and biophysics,
J Chang, and
H Jaeschke, and
K Randerath
December 1992,
Biochemical pharmacology,
J Chang, and
H Jaeschke, and
K Randerath
November 2003,
Molecular pharmacology,
J Chang, and
H Jaeschke, and
K Randerath
January 2013,
Methods in enzymology,
J Chang, and
H Jaeschke, and
K Randerath
April 1982,
The Journal of biological chemistry,
