ATP breakdown and resynthesis in the development of gastrointestinal mucosal damage and its prevention in animals and human (an overview of 25 years ulcer research studies).
The changes in membrane-bound ATP systems (breakdown and resynthesis) were analyzed in different experimental ulcer models (such as ETOH, HCl, NaOH, 25% NaCl-induced, pyloric ligated + epinephrine treated, stress, reserpine treated, indomethacin treated rat models) and chronic antral, duodenal and jejunal ulcers in patients. The energy system parameters (adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), cyclic AMP (cAMP), lactate) were measured from different sites of gastrointestinal mucosa, and values of ATP/ADP, adenylate pool (ATP + ADP + AMP) and energy charge ((ATP + 0.5 ADP)/(ATP + ADP + AMP)) were calculated. The biochemical measurements were done at different times during the development of gastrointestinal mucosal lesions, without and with application of different drugs (PGI2, atropine, cimetidine) and bilateral surgical vagotomy. The aims of our present paper were: 1.) To summarize the main directions of ATP breakdown during the development of gastrointestinal lesions or ulcers in different experimental models and human beings: 2.) To summarize the biochemical steps of defense of gastrointestinal mucosa against chemicals, drugs or unknown pathogenic factors; 3.) To analyze the importance of membrane-bound ATP-dependent energy systems in order to understand the mucosal lesions and their prevention; 4.) To evaluate the real values of changes in these parameters from the point of view of ulcerogenesis and its prevention; 5.) To find some correlation between the energy parameters during mucosal damage and its prevention: 6.) To understand better the types of tissue reactions (metabolic) due to development of mucosal lesions and prevention.(ABSTRACT TRUNCATED AT 400 WORDS)
Mózsik
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First Department of Medicine, Medical University, Pécs, Hungary.
Király
A
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Sütö
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Vincze
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A
D000255:Adenosine Triphosphate / Q000096:biosynthesis / Q000378:metabolism*; D000818:Animals; D001241:Aspirin; D001285:Atropine / Q000494:pharmacology; D002199:Capillary Permeability / Q000502:physiology; D005260:Female; D005502:Food; D005753:Gastric Mucosa / Q000378:metabolism / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D010437:Peptic Ulcer / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D012110:Reserpine; D013217:Starvation / Q000378:metabolism; D013315:Stress, Psychological / Q000503:physiopathology; D014628:Vagotomy
D001285:Atropine; D012110:Reserpine; D000255:Adenosine Triphosphate; D005947:Glucose; D001241:Aspirin