scholarly journals Metabolism of polycyclic compounds. 26. The hydroxylation of some aromatic hydrocarbons by the ascorbic acid model hydroxylating system and by rat-liver microsomes

1964 ◽  
Vol 92 (3) ◽  
pp. 631-638 ◽  
Author(s):  
E Boyland ◽  
M Kimura ◽  
P Sims
1965 ◽  
Vol 97 (1) ◽  
pp. 247-249 ◽  
Author(s):  
NC Ghosh ◽  
I Chatterjee ◽  
GC Chatterjee

1. The synthesis of l-ascorbic acid from either d-glucuronolactone or l-gulonolactone by liver microsomes of rats is decreased under conditions of hypervitaminosis A; under hypervitaminosis D the synthesis from d-glucuronolactone is increased and that from l-gulonolactone is not affected. 2. The microsomal conversion of l-gulonolactone into l-ascorbic acid is impaired in liver tissues of rats made deficient with respect to either vitamin A or vitamin D when compared with the controls maintained on stock diet.


1989 ◽  
Vol 258 (2) ◽  
pp. 617-620 ◽  
Author(s):  
O I Aruoma ◽  
B Halliwell ◽  
M J Laughton ◽  
G J Quinlan ◽  
J M C Gutteridge

When Fe2+ ions are added to rat-liver microsomes, lipid peroxidation begins after a short lag period. Fe2+-dependent peroxidation in the first few minutes of the incubation can be increased by adding Fe3+, ascorbic acid or Pb2+ ions; these stimulations are not additive. By contrast, Pb2+ ions inhibit peroxidation of microsomes in the presence of Fe3+/ascorbate or Fe3+-ADP/NADPH. In liposomes made from ox-brain phospholipids, Fe2+-dependent peroxidation is stimulated slightly by Fe3+, but much more so by ascorbic acid, Al3+ or Pb2+; these stimulations are not additive. Liposomal peroxidation in the presence of Fe3+/ascorbate is inhibited by Pb2+ or Al3+. These results argue against the participation of an Fe2+-Fe3+-O2 complex, or a critical 1:1 ratio of Fe2+ to Fe3+, in the initiation of lipid peroxidation in liposomes and rat-liver microsomes.


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