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PubMedDate not supplied

Parietal cells in duodenal ulcer disease: a histochemical study of the effects of omeprazole and ranitidine on mitochondrial activities.

H2-Receptor antagonists and omeprazole, a H-K ATPase inhibitor, inhibit acid secretion from the parietal cells. The ultrastructural changes of the parietal cells after treatment have been described, but the changes in the mitochondrial activity which reflect the energetic metabolism were not well defined. To study the effect of omeprazole and H2-receptor antagonists on the mitochondrial activity of the parietal cells, endoscopic biopsies were taken from nine patients with duodenal ulcer before and after treatment with either 10 mg or 20 mg omeprazole each morning, or 150 mg ranitidine twice daily for 2 weeks, given in a double-blind randomized manner. Three patients with healed duodenal ulcer who were on maintainence treatment with 150 mg ranitidine nightly for 1 year had an endoscopy performed after 4 and 12 months and two non-ulcer dyspeptic patients were recruited as controls. Three biopsies were taken during each endoscopy from the body of the stomach. The mitochondrial activity was assessed by the reaction of succinic dehydrogenase with nitroblue tetrazolium and of cytochrome oxidase with naphthoic acid mixed with N-phenyl-p-phenylenediamine, according to the intensity of the staining reaction. After treatment with omeprazole or ranitidine, the mitochondrial activity decreased appreciably and returned to the pretreatment level on cessation of treatment. Patients on maintainence ranitidine showed decreased mitochondrial activities after 4 months, which, however, returned to pretreatment levels in two patients. It is concluded that short-term treatment with omeprazole or ranitidine resulted in reversible suppression of mitochondrial activity while long-term treatment with ranitidine resulted in an initial suppression followed by a tendency to return to pretreatment level despite continued treatment.

Adult↗
PubMed1985

Neurochemical and histochemical characterization of neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on brain catecholamine neurones in the mouse.

Systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused a rapid and long-lasting reduction of both 3,4-dihydroxyphenylalanine (dopamine, DA) and noradrenaline (NA) in mouse brain, as observed histo- and neurochemically. The depleting effects were more pronounced after repeated MPTP administration and the most marked reductions were observed after 2 X 50 mg MPTP/kg s.c., when DA in striatum and NA in frontal cortex were reduced by greater than 90% 1 week after MPTP. Mice with such catecholamine depletions were markedly sedated and almost completely immobilized. The behavioural syndrome after MPTP resembled that seen after reserpine, a monoamine-depleting drug. MPTP also caused a long-lasting reduction of catecholamine uptake in striatal DA and cortical NA nerve terminals and reduced tyrosine hydroxylase activity in these regions. There was no evidence that MPTP caused any marked DA and NA cell body death. MPTP given acutely transiently elevated serotonin levels. The results are compatible with a neurotoxic action of MPTP on both DA and NA nerve terminals. The nigro-striatal DA and the locus coeruleus NA neurone systems appeared to be most susceptible. Synthesis and utilization of residual striatal DA and cortical NA were increased, as often observed in partially denervated monoamine-innervated brain regions. Both DA and NA showed a gradual recovery, which took months to become complete and may have been related to a regrowth of catecholamine nerve terminals.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2006

Histometric and histochemical analysis of the effect of trichloroacetic acid concentration in the chemical reconstruction of skin scars method.

BACKGROUND: Atrophic scars can be induced by various causes, including severely inflamed acne, chicken pox, and trauma. Many treatment modalities are used for reconstructing and improving the appearance of scars with various treatment results. OBJECTIVE: A recent report shows the clinical efficacy of the chemical reconstruction of skin scars (CROSS) method, which consists of the focal application of trichloroacetic acid (TCA) in a higher concentration. Histometric analysis of the CROSS method, however, has not yet been established. METHODS: In this study, five hairless mice were used to evaluate the effect of the CROSS method and to analyze the difference between the CROSS method and simple TCA application. RESULTS: Similar histologic changes were observed in the two methods, including epidermal and dermal rejuvenation with new collagen deposition. These changes, however, were more prominent in the CROSS method-treated areas, particularly when 100% TCA was used. CONCLUSION: The results of this study suggest that treatment of atrophic scars using the CROSS method is more effective than simple application of TCA in activating fibroblasts in the dermis and increasing the amount of collagen.

Administration, Topical↗
PubMed1985

Structural and histochemical study of the effect of 1,25-dihydroxyvitamin D3 on long-bone growth center in suckling mice.

The in vivo effects of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] on cellular structure and response, matrix metachromasia and mineralization have been studied in the epiphysis and growth plate of humeri in normal neonatal mice. A relatively low dose of the metabolite, 50 ng/kg body weight, significantly increased the overall size of humeral growth plate, the zone of proliferating cells and that of hypertrophic chondrocytes. The response of the tissue to the metabolite changed with the increase in dose administered so that it was only the zone of proliferation that still showed increases in size in comparison to untreated controls. 1,25 (OH)2D3 led to an increase in the metachromatic reaction of the cartilage matrix in the chondroblastic zone, and to marked increase in matrix mineralization in the hypertrophic zone. Qualitative changes were also noted in the structure of chondroblasts and hypertrophic chondrocytes. 1,25(OH)2D3 affected the osteoblastic and osteocytic populations of cells along the metaphysis and diaphysis of the humerus. High doses of 1,25(OH)2D3 brought about distinct atrophic changes in the above cells. Chondrocytes in the epiphysis were found to synthesize type I collagen and fibronectin. These findings indicate that excessive doses of 1,25(OH)2D3 in an intact growing animal affect the normal differentiative pathway of prechondroblasts and thereby affect long bone development.

Animals↗