title: Effects of adaptive exercise on apoptosis in cells of rat renal tubuli.
abstract: Regular exercise is known to improve physiological and functional capacity of many organs due to adaptive processes. We have previously shown that acute exercise in untrained rats results in apoptosis of renal tubular cells and that the apoptotic process seems to be associated with stimulation of angiotensin II, AT1 and AT2 receptors. In this study, we examined the influence of regular training on apoptosis and the role of angiotensin II receptors and antioxidant enzymes in mediating the adaptive response in renal tubular cells. We measured apoptosis, expression of AT1 and AT2 receptors, level of lipid peroxidation (TBARS) and activities of antioxidant enzymes, SOD, GPx and CAT in kidneys of sedentary rats that were exposed to acute exercise and rats that were trained for 8 weeks. In untrained animals, the acute exercise resulted in increased apoptosis and increased expression of AT1 and AT2 receptors in renal tubular cells, while in the rats exposed to the 8-week regular training, there were no changes in apoptosis nor AT1 and AT2 receptor expression as compared to the sedentary animals. The TBARS levels were significantly increased in acutely exercised rats, while in rats pre-exposed to the training they remained unchanged. The acute exercise, as well as regular training, did not change SOD, CAT or GPx activities. These findings suggested that the acute exercise-induced apoptosis in renal tubules could involve action of AT1 and AT2 receptors as well as oxidative stress, while the regular training was shown to prevent apoptosis in renal tubular cells via modulated expression of AT1 and AT2 receptors.
authors.affiliation: Department of Histology and Embryology, Medical University of Wroclaw, Wroclaw, Poland. mapod@hist.am.wroc.pl
authors.forename: Marzena
authors.initials: M
authors.lastname: Podhorska-Okolow
authors.forename: Piotr
authors.initials: P
authors.lastname: Dziegiel
authors.forename: Eugenia
authors.initials: E
authors.lastname: Murawska-Cialowicz
authors.forename: Jolanta
authors.initials: J
authors.lastname: Saczko
authors.forename: Julita
authors.initials: J
authors.lastname: Kulbacka
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Gomulkiewicz
authors.forename: Katia
authors.initials: K
authors.lastname: Rossini
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Jethon
authors.forename: Ugo
authors.initials: U
authors.lastname: Carraro
authors.forename: Maciej
authors.initials: M
authors.lastname: Zabel
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000378:metabolism; D007686:Kidney Tubules, Distal / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase