Ozone treatment reduces markers of oxidative and endothelial damage in an experimental diabetes model in rats.
Ozone has been used as a therapeutical agent and beneficial effects have been observed. However so far only a few biochemical and pharmacodynamic mechanisms have been elucidated. We demonstrate that controlled ozone administration may promote an oxidative preconditioning or adaptation to oxidative stress, preventing the damage induced by reactive oxygen species (ROS). Taking into account that diabetes is a disorder associated with oxidative stress, we postulate that ozone treatment in our experimental conditions might protect antioxidant systems and maintain, at a physiological level, other markers of endothelial cell damage associated with diabetic complications. Five groups of rats were classified as follows: (1) control group treated only with physiological saline solution; (2) positive control group using streptozotocin (STZ) as a diabetes inductor; (3) ozone group, receiving 10 treatments (1.1 mg kg(-1)), one per day after STZ-induced diabetes; (4) oxygen group (26 mg kg(-1)), one per day, as in group 3 but using oxygen only; (5) control ozone group, as group 3, but without STZ. The ozone treatment improved glycemic control and prevented oxidative stress, the increase of aldose reductase, fructolysine content and advanced oxidation protein products. Nitrite and nitrate levels were maintained without changes with regard to non-diabetic control. The results of this study show that repeated administration of ozone in non-toxic doses might play a role in the control of diabetes and its complications.
Al-Dalain
S M
SM
Center for Research and Biological Evaluation (CIEB-IFAL), University of Havana, Havana 10400, Cuba.
Martínez
G
G
Candelario-Jalil
E
E
Menéndez
S
S
Re
L
L
Giuliani
A
A
León
O S
OS
D000818:Animals; D015415:Biomarkers / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D006031:Glycosylation / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis; D009573:Nitrites / Q000378:metabolism; D010083:Oxidants, Photochemical / Q000494:pharmacology* / Q000627:therapeutic use; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D010126:Ozone / Q000008:administration & dosage / Q000627:therapeutic use*; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D010083:Oxidants, Photochemical; D011506:Proteins; D009569:Nitric Oxide; D010126:Ozone