Soluble semicarbazide-sensitive amine oxidase (SSAO) activity is related to oxidative stress and subchronic inflammation in streptozotocin-induced diabetic rats.
Diabetes is known to increase the risk of Alzheimer's disease (AD) and vascular dementia via oxidative stress and inflammation. There are speculations that SSAO activity might be related to the development of AD. Our aim was to investigate whether changes of soluble SSAO activity, oxidative stress and inflammation markers are related to each other in diabetes. Soluble and tissue-bound SSAO activities (from serum and aorta, respectively) were determined in streptozotocin (STZ)-induced diabetic rats without insulin treatment, receiving insulin once, or twice daily compared to control animals. After three weeks of treatment soluble and tissue-bound SSAO activities (seSSAO and aoSSAO, respectively), serum total antioxidant status (TAS), high sensitivity C-reactive protein (hsCRP), fructose amine levels and routine laboratory parameters were determined. SeSSAO activity significantly increased in the diabetic groups without treatment and receiving insulin once daily, and a marked decrease in aoSSAO activity was seen in all diabetic groups. Increased oxidative stress was correlated with hsCRP elevation, while hsCRP and seSSAO activity were also significantly correlated. In all groups seSSAO and aoSSAO activities were in negative correlation with each other. Our results support the view that poor metabolic control leads to increased oxidative stress, which in turn may cause the elevation of hsCRP levels. Soluble SSAO on the one hand acts as an adhesion molecule--thus possibly being a factor responsible for the late complications of diabetes--and on the other hand, it may contribute to oxidative stress. Our parsimonious conclusion is that there is a relation between the risk factors of AD and vascular dementia (diabetes, oxidative stress and chronic inflammation) and SSAO activity, which may originate from the vessel wall.
Somfai
Gábor Márk
GM
Faculty of Medicine, 2nd Department of Ophthalmology, Semmelweis University, Mária str. 39, H-1085 Budapest, Hungary. somfaigm@szem2.sote.hu
Knippel
Barbara
B
Ruzicska
Eva
E
Stadler
Krisztián
K
Tóth
Miklós
M
Salacz
György
G
Magyar
Kálmán
K
Somogyi
Anikó
A
D000544:Alzheimer Disease / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D006631:Amine Oxidase (Copper-Containing) / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D002536:Cerebral Arteries / Q000378:metabolism / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000378:metabolism / Q000503:physiopathology; D002908:Chronic Disease; D015140:Dementia, Vascular / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D048909:Diabetes Complications / Q000378:metabolism* / Q000503:physiopathology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D004789:Enzyme Activation / Q000502:physiology; D005632:Fructose / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012995:Solubility; D015854:Up-Regulation / Q000502:physiology
D000975:Antioxidants; D005632:Fructose; D002097:C-Reactive Protein; D006631:Amine Oxidase (Copper-Containing)