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Crypt fission in the small intestine and colon. A mechanism for the emergence of G6PD locus-mutated crypts after treatment with mutagens.

In the small intestine and colon, administration of mutagens leads to the emergence of crypts populated by cells with a different, mutated phenotype. This is preceded by a transient rise in the frequency of crypts with a partially mutated phenotype, and the disappearance of these partially mutated crypts occurs contemporaneously with the attainment of a plateau value of the wholly mutated crypts. Here, using the mutagen ethyl nitrosourea and loss of glucose-6-phosphate dehydrogenase staining as a marker, we show that the plateau is reached at between 4.6 and 7 weeks in the colon and at 12 weeks in the small intestine of the same mice. Explanations for this difference have included differences in the stem cell cycle time of a single "master" stem cell or multiple stem cells occupying a stem cell "niche" with random loss after stem cell division. However, we demonstrate that the crypt fission index, or the incidence of crypts in fission, is some four times higher in the colon than in the small intestine at the time of ethyl nitrosourea injection, and propose an alternative hypothesis based on crypt fission as the mechanism for the more rapid evolution of wholly mutated crypts in the colon. The hypothesis should enable us to predict the results of future experiments, namely that the emergence of wholly mutated crypts is proportional to the crypt fission index.

Animals↗

[Hemoglobin abnormalities and glucose 6 phosphate dehydrogenase deficiency (G6PD) in 101 refugees from southeast Asia].

Hematological studies were performed systematically in 101 refugees from South-Eastern Asia living in the Grenoble area at the present time. We found: --4 haemoglobin E homozygosity, --29 haemoglobin E heterozygosity, --2 beta-thalassemia heterozygosity, --4 alpha-thalassemia heterozygosity, --14 glucose 6 phosphate dehydrogenase deficiencies.

Asia, Southeastern↗

Levels of erythrocyte malonyldialdehyde, vitamin E, reduced glutathione, G6PD activity & plasma urate in patients of pregnancy induced hypertension.

To assess the oxidative stress across the cell membrane in patients suffering from pregnancy induced hypertension, erythrocyte malonyldialdehyde, vitamin E, reduced glutathione, glucose-6-phosphate dehydrogenase activity and plasma urate levels were estimated in 25 non pregnant women, 40 normotensive pregnant women and 40 women with pregnancy induced hypertension (PIH). As compared to non pregnant women, there was a significant increase in the levels of erythrocyte malonyldialdehyde and plasma urate in normotensive pregnant women, which were further increased in women with PIH. Erythrocyte glutathione levels were raised in normotensive pregnant women as compared to non pregnant women. Its levels were decreased in patients of PIH as compared to normotensive pregnant women. Cellular bio-availability of vitamin E was depressed in both normotensive pregnancy as well as patients with pregnancy induced hypertension as compared to non pregnant women.

Adult↗

G6PD deficiency.

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Anemia, Hemolytic↗

Acalypha indica induced haemolysis in G6PD deficiency.

Four patients who developed acute intravascular haemolysis after ingestion of a broth containing Acalypha indica (Sinhala: Kuppameniya) are reported. All four patients were found to have glucose-6-phosphate dehydrogenase deficiency. It is a common belief that ayurvedic medicines are free of side effects. Our report confirms again the fallacy of this belief.

Child↗