INVESTIGADORES
EVELSON Pablo Andres
congresos y reuniones científicas
Título:
Lung oxygen metabolism after an acute exposure to ambient particles
Autor/es:
MAGNANI, NATALIA; MARCHINI, TIMOTEO; TASAT, DEBORAH; ALVAREZ, SILVIA; EVELSON, PABLO
Lugar:
Sao Pedro
Reunión:
Congreso; VII Meeting of the Society for Free Radical Biology and Medicine South American Group; 2011
Institución organizadora:
Society for Free Radical Biology and Medicine South American Group
Resumen:
Reactive oxygen
species are able to initiate molecular mechanisms leading to lung oxidative
damage due to particulate matter exposure. The aim of this work was to study
the O2 metabolism in mice lung after an acute exposure to ambient
particles (ROFA) by intranasal instillation (1.00 mg/kg body). Oxygen consumption
by tissue cubes was determined by a polarographic technique. As main sources of
oxygen uptake, we assessed NADPH oxidase activity in homogenates, following the
superoxide anion (O2.-) production and NADPH consumption,
and mitochondrial O2 consumption. Respiratory complexes activity and
H2O2 production were also measured in isolated
mitochondria by spectrophotometric and fluorometric assays respectively. Measurements
were made 1 h after instillation. ROFA exposure showed a 66% increased tissue O2
consumption (control: 225 ± 7 ng-at O/min. g tissue p<0.01). O2
uptake inhibition by KCN in ROFA group was found to be 45%, while for control
group was 59%. NADPH oxidase activity showed similar increases through both
assays, O2.- production (25%) (control: 0.72 ± 0.02 AU/mg
prot. p<0.01), and NADPH consumption (32%) (control: 0.82 ± 0.09 nmol
NADPH/min. mg prot. p<0.01) after particle instillation. After ROFA
exposure, mitochondria showed a 33% increased in state 3 O2
consumption (control: 107 ± 4 ng-at O/min. mg prot. p<0.01), no differences
in state 4, no significant differences in H2O2 production,
and increased complex II activity by 25% (control: 14.1 ± 0.74 nmol /min. mg
prot. p<0.01). Our data shows that increased tissue O2 consumption
is caused by increased mitochondria O2 uptake, through a higher
complex II activity, and an augmented NADPH oxidase activity, due to an
inflammatory response.