Biomedical Engineering Reference
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O 2 -dependent manner but also in the absence of O 2 (Fig. 8.9), leading to the hypothesis
that while this process may prevent H 2 S toxicity of cytochrome oxidase, it may also pro-
vide electrons and protons for oxidative phosphorylation, thus perhaps sparing carbohy-
drates for other use [5]. Under air-equilibrated conditions, mitochondrial H 2 S consumption
was accompanied by simultaneous increased O 2 consumption, leading some investigators
to use H 2 S-stimulated O 2 consumption as an indirect and largely qualitative measure of
H 2 S consumption. Using the PHSS to measure H 2 S consumption directly in combina-
tion with O 2 consumption provided a dynamic metabolic stoichiometry of H 2 S to O 2 con-
sumption over a range of O 2 levels as well as demonstrated that H 2 S can be consumed in
the absence of O 2 . This detailed assessment of mitochondrial H 2 S metabolism provided
evidence of specifi c enzymatic steps and insight into mammalian H 2 S metabolism.
8.6.2.2 Cultured cells, intact tissues and organs
To determine cellular H 2 S consumption rates, bolus additions of known H 2 S concentra-
tions were added to the respirometer chamber with or without rat aorta smooth muscle
12.5
m sulfide
(a)
8
15
6
10
4
5
2
0
0
10
10
(b)
8
8
6
6
4
4
2
2
0
0
0
20
40
60
80
100
120
140
Time, min
FIGURE 8.9 Mitochondrial O 2 and H 2 S consumption from non-limiting O 2 to anoxic conditions. (a)
Isolated mitochondria were exposed to repeated bouts of 12.5 µM H 2 S until anoxia was achieved. (b) At
higher O 2 levels, both O 2 and H 2 S consumption events are coincident, but as the O 2 levels decline the events
become uncoupled and O 2 consumption is limited fi rst. The multiphasic kinetics of O 2 consumption may
result from transient inhibition of cytochrome c oxidase by H 2 S. Under anoxia, H 2 S consumption continues
at a low level (after [36]; reproduced with permission of the Company of Biologists).
 
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