Wood smoke exposure induces a decrease in respiration parameters and in the activity of respiratory complexes I and IV in lung mitochondria from guinea pigs

Abstract

Domestic exposure to biomass smoke represents the second cause of chronic obstructive lung disease. Previous studies have shown that exposure of guinea pigs to wood smoke is capable of generating oxidative stress in lung tissue, and this may involve a failure at a mitochondrial level, given its close relation with the production of reactive oxygen species (ROS). The purpose of this study was to evaluate, in guinea pigs exposed to wood smoke, the lung mitochondrial functionality through O2 consumption measurement and the determination of the mitochondrial complexes enzymatic activity. We found that normal and maximum respiration decreased at 15 and 30 min of wood smoke exposure, recovering its normal values at 180 min. The same behavior was observed for the respiratory control rate (RCR) and the ADP/O value. Complex I activity decreased significantly after 30 min of exposure and it returned to baseline after 180 min. The greatest alteration was observed by the decrease of 85% on complex IV activity at 30 min of exposure, which returned to control values after 180 min of exposure. It is concluded that even when wood smoke exposure induces severe mitochondrial respiration alterations at the first 30 min, it seems that there is one or many ways by which mitochondria can reinstate its normal function after 180 min of exposure.

Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells

“…Additionally, there might be dose-dependent and also cell type-dependent responsiveness between alveolar and bronchial epithelial cells to CSE. Furthermore, a time dependency was observed in wood smoke-treated guinea pigs showing early decrease of mitochondrial function but full recovery and overcompensation later on (17). In our study, we cannot rule out that mitochondrial function is transiently decreased at earlier time points than 6 h and improves later.…”

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

“…The ratio of states 3/4, known as respiratory control ratio (RCR), was calculated; this ratio expresses the coupling degree between ETC and ATP synthesis. The ADP/oxygen (ADP/O) ratio was also calculated; this is another important mitochondrial functionality parameter that expresses the relationship between the amount of added ADP (mol) and the consumed oxygen (mol) during state 3 [33]. Measurement of mitochondrial respiration was performed using a Clarktype electrode (Strathkelvin Instruments, ML, Scotland) at 37°C.…”

“…Measurement of mitochondrial respiration was performed using a Clarktype electrode (Strathkelvin Instruments, ML, Scotland) at 37°C. Mitochondria (15 lg of protein) were suspended in 100 lL of respiration buffer, which contain 70 mM sucrose, 220 mM mannitol, 1 mM Na 2 EDTA, 10 mM K 2 HPO 4 , 5 mM HEPES, 5 mM MgCl 2 , 0.2 % BSA; pH 7.2 [33]. To evaluate respiration driven by complex I, 10 mM glutamate ?…”

“…Renal mitochondria were isolated using Percoll Ò gradients, based mainly in a lung mitochondria isolation method with minor modifications [33]. The animals were euthanized, and both kidneys were immediately rinsed in cold isolation buffer with the following composition: 225 mM D-mannitol, 75 mM sucrose, 1 mM Na 2 EDTA, 11 mM HEPES, and 0.1 % BSA, pH 7.4.…”

Evaluation of oxidative stress and whole blood viscosity for clinical laboratory testing of smoking toxicity

“…6 Also, industrial and household smoke could cause oxidative stress, which would go on to induce hyperviscosity. [7][8][9] Therefore, there is an obvious need to develop a unified approach for assessment of cigarette toxicity, especially for non-smokers, because this group is exposed to second-hand smoke and also third-hand smoke that is the accumulation of first-hand smoke over a period becoming more toxic in the process. 5,10 Also, since tobacco causes a duration-dependent increase in oxidative stress, this impacts on toxicity.…”