Acute exercise in ozone-polluted air induces apoptosis in rat quadriceps femoris muscle cells via mitochondrial pathway.

Ozone (O3) pollution can decrease sport performance and induce respiratory toxicity, but relatively few studies have investigated its effects on skeletal muscles. We randomly assigned rats to the following groups based on a 2 â€‹× â€‹4 two-factor factorial design: Air+0, Air+10, Air+15, and Air+20, O3+0, O3+10, O3+15, and O3+20. The rats in the +0 groups rested, whereas those in the +10, +15, and +20 groups ran on a treadmill (in clean air for Air groups and in air polluted with 0.14 â€‹parts per million [ppm] O3 for O3 groups) at speeds of 10, 15, and 20 â€‹m/min, respectively, for 1 â€‹h. Thereafter, key enzyme activities involving the tricarboxylic acid cycle, oxidative phosphorylation, adenosine triphosphate (ATP) content, histopathological changes, oxidative stress, inflammation factors, and apoptosis were assessed in the rat quadriceps femoris samples. Ozone reduced key enzyme activities and ATP contents in the quadriceps femoris regardless of whether the rats exercised. Pathological changes, inflammatory factors, oxidative stress, and mitochondria-dependent apoptosis were only evident under conditions of exercise combined with ozone and increasingly worsened as exercise intensity increased. These findings suggested that acute exercise under ozone exposure could induce damage to the quadriceps femoris, which would negatively affect sport performance. Ozone-induced disrupted energy metabolism might be an early event that becomes more critical as exercise intensity increases. Therefore, care should be taken when exercising in polluted air, even when ozone pollution is mild.

Altered lipidomic profiles in lung and serum of rat after sub-chronic exposure to ozone.

Ozone (O) exposure not only causes lung injury and lung inflammation but also changes blood composition. Previous studies have mainly focused on inflammatory processes and metabolic diseases caused by acute or chronic ozone exposure. However, the effect of ozone on lipid expression profiles remains unclear. This study aimed to investigate the lipidomic changes in lung tissue and serum of rats after ozone exposure for three months and explore the lipid metabolic pathway involved in an ozone-induced injury. Based on the non-targeted lipidomic analysis platform of the UPLC Orbitrap mass spectrometry system, we found that sub-chronic exposure to ozone significantly changed the characteristics of lipid metabolism in lungs and serum of rats. First, the variation in sphingomyelin (SM) and triglyceride (TG) levels in the lung and serum after O3 exposure are shown. SM decreased in both tissues, while TG decreased in the lungs and increased in the serum. Further, the effect of ozone on glycerophospholipids in the lung and serum was completely different. Phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylinositol (PI) were the major glycerophospholipids whose levels were altered in the lung, while phosphatidylglycerol (PG), phosphatidic acid (PA), and phosphatidylcholine (PC) levels changed dramatically in the serum. Third, after O3 exposure, the level of monogalactosyldiacylglycerol (MGDG), mainly MGDG (43, 11), a saccharolipid, declined significantly and uniquely in the serum. These results suggested that sub-chronic O3 exposure may play a role in the development of several diseases through perturbation of lipidomic profiles in the lungs and blood. In addition, changes in the lipids of the lung and blood may induce or exacerbate respiratory diseases.