Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Wistar male rats weighing 230-250 g were given 10 mg aminopyrine and 10 mg sodium nitrite daily, by gavage, for 20 days. The histological changes in the liver are of the cirrhotic type. The ultrastructural changes are dependent on the hepatocyte position in the hepatic structural changes are dependent on the hepatocyte position in the hepatic lobule. Thus, in the perilobular area one finds hepatocytes with an increased volume and hypertrophic nuclei and nucleoli, mitochondriae swollen with dispersed cristae, decrease of the number of free ribosomes, glycogen depletion, GER decrease and SER development. In the centrolobular area, the most injured, there are necrotic changes with numerous cytolysosomal formations. The histoenzymological results show a decrease of LDH, SDH, CyOx, GtDH, StDH, ATP-ase and G6P activities. The activity of Ac.P on the contrary, is greater in the intoxicated rats, which correlates with the above-mentioned necrobiosis processes.
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PMID:Histoenzymological and ultrastructural changes in rats following the administration of aminopyrine and nitrite (nitrosoaminopyrine). 626 34

Omeprazole, a proton pump inhibitor used to treat peptic ulcer and gastroesophageal reflux disease, has been associated to chronic kidney disease and acute interstitial nephritis. However, whether omeprazole is toxic to renal cells is unknown. Omeprazole has a lethal effect over some cancer cells, and cell death is a key process in kidney disease. Thus, we evaluated the potential lethal effect of omeprazole over tubular cells. Omeprazole induced dose-dependent cell death in human and murine proximal tubular cell lines and in human primary proximal tubular cell cultures. Increased cell death was observed at the high concentrations used in cancer cell studies and also at lower concentrations similar to those in peptic ulcer patient serum. Cell death induced by omeprazole had features of necrosis such as annexin V/7-AAD staining, LDH release, vacuolization and irregular chromatin condensation. Weak activation of caspase-3 was observed but inhibitors of caspases (zVAD), necroptosis (Necrostatin-1) or ferroptosis (Ferrostatin-1) did not prevent omeprazole-induced death. However, omeprazole promoted a strong oxidative stress response affecting mitochondria and lysosomes and the antioxidant N-acetyl-cysteine reduced oxidative stress and cell death. By contrast, iron overload increased cell death. An adaptive increase in the antiapoptotic protein BclxL failed to protect cells. In mice, parenteral omeprazole increased tubular cell death and the expression of NGAL and HO-1, markers of renal injury and oxidative stress, respectively. In conclusion, omeprazole nephrotoxicity may be related to induction of oxidative stress and renal tubular cell death.
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PMID:Molecular pathways driving omeprazole nephrotoxicity. 3209 86