TY - JOUR
T1 - Effects of short-term ozone exposure on lung mitochondrial oxidative and energy metabolism
AU - Mustafa, Mohammad G.
AU - Cross, Carroll E
PY - 1974
Y1 - 1974
N2 - Ozone effects on lung mitochondrial oxidative metabolism were examined after short-term exposure of rats and monkeys to O3. Exposure of animals to 2 ppm O3 for 8 hr or to 4 ppm O3 for 4 hr caused a 15-27% (P < 0.05) depression of lung mitochondrial O2 consumption, using 2-oxoglutarate, succinate, and glycerol-1-phosphate. but not ascorbate plus Wurster's blue as substrates. Under these exposure conditions (4 ppm 4 hr) the ADP:O ratios dropped 25-36% (P < 0.05) and the respiratory control indices decreased 27-33% (P < 0.02) for oxidation of all substrates examined. Lung mitochondria from control animals were relatively impermeable to added NADH, but those from O3-exposed animals showed an increased permeability as judged from NADH oxidation at a rate 3-fold higher than the control. Likewise, added cytochrome c caused a 22% (P < 0.01) stimulation of succinate oxidation in exposed lung mitochondria as against 5% (nonsignificant) in controls. Ozone exposure also caused a 20% (P < 0.01) oxidation of thiol groups in lung mitochondria, but no lipid peroxidation products were detectable in O3-exposed lung tissue. The depression of substrate utilization, coupled phosphorylation and respiratory control observed in lung mitochondria of O3-exposed animals might be related to alteration of membrane permeability, and inhibition of respiratory enzymes (dehydrogenases) due to oxidation of functional thiol groups.
AB - Ozone effects on lung mitochondrial oxidative metabolism were examined after short-term exposure of rats and monkeys to O3. Exposure of animals to 2 ppm O3 for 8 hr or to 4 ppm O3 for 4 hr caused a 15-27% (P < 0.05) depression of lung mitochondrial O2 consumption, using 2-oxoglutarate, succinate, and glycerol-1-phosphate. but not ascorbate plus Wurster's blue as substrates. Under these exposure conditions (4 ppm 4 hr) the ADP:O ratios dropped 25-36% (P < 0.05) and the respiratory control indices decreased 27-33% (P < 0.02) for oxidation of all substrates examined. Lung mitochondria from control animals were relatively impermeable to added NADH, but those from O3-exposed animals showed an increased permeability as judged from NADH oxidation at a rate 3-fold higher than the control. Likewise, added cytochrome c caused a 22% (P < 0.01) stimulation of succinate oxidation in exposed lung mitochondria as against 5% (nonsignificant) in controls. Ozone exposure also caused a 20% (P < 0.01) oxidation of thiol groups in lung mitochondria, but no lipid peroxidation products were detectable in O3-exposed lung tissue. The depression of substrate utilization, coupled phosphorylation and respiratory control observed in lung mitochondria of O3-exposed animals might be related to alteration of membrane permeability, and inhibition of respiratory enzymes (dehydrogenases) due to oxidation of functional thiol groups.
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U2 - 10.1016/0003-9861(74)90219-7
DO - 10.1016/0003-9861(74)90219-7
M3 - Article
C2 - 4366422
AN - SCOPUS:0016186809
VL - 162
SP - 585
EP - 594
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 2
ER -