Butyrate-induced cell death and differentiation are associated with distinct patterns of ROS in HT29-derived human colon cancer cells.

To investigate the role of reactive oxygen species (ROS) induced by butyrate in tumor cells, we compared HT29R, an HT29-derived human colon cancer cell line refractory to butyrate-induced cell differentiation but highly sensitive to cell death, with the differentiation-positive HT29-12 and HT29-21 cell lines (exhibiting low sensitivity to butyrate-induced cell death), with respect to levels of butyrate-induced free radicals (FRs), ROS, and H(2)O(2). Dose-dependent increase of FRs (as determined by electron spin resonance spectroscopy) and ROS (dichlorofluorescein assay) was induced in HT29R, but not in HT29-12 and HT29-21 cells, where, in contrast to HT29R, a dose-dependent increase of H(2)O(2) release (phenol red assay) was induced by butyrate. The mode of butyrate-induced cell death in HT29R cells was of a mixed type with necrosis predominating, which, however, switched to apoptosis as the major type of cell death in the presence of the drugs 1,5-dihydroxyisoquinoline, resveratrol, or cyclosporine A.

Effect of hydrogen peroxide on interleukin-8 synthesis and death of Caco-2 cells.

Intestinal epithelial cells can secrete interleukin-8 (IL-8), among other substances in response to different stimuli, which plays an important role in mucosal immune response. Above a certain concentration range, hydrogen peroxide causes cell death by necrosis or apoptosis. We investigated the time- and dose-dependent induction of IL-8 by hydrogen peroxide in the human colon adenocarcinoma cell line Caco-2.

[Changes of authorship characteristics in Hungarian medical publications in the period of 1967-97].

Authorship characteristics of publications appeared in the 1967-1977-1987-1997 volumes of the Orvosi Hetilap (Medical Weekly) were analysed and compared with corresponding data in the international medical literature. Following results were achieved: 1. The total number of medical publications gradually decreased although the number of pages of the volumes steadily increased during the period studied; this could be explained rather by a changed structure or editorial policy than by lowering of the readiness for publishing.

[Pathogenetic aspects of acute renal insufficiency in experimental acute pancreatitis].

The authors carried out a study of some pathogenic mechanisms related to the development of acute renal failure in animals following pancreatitis-induced shock. The study was made in 110 white rats in which acute pancreatitis was induced experimentally, and the results were compared with those obtained in a control lot of 40 rats. The behaviour of some biochemical parameters was investigated (cathecholamines, acid phosphatases, catepsine, aminoacids and polypeptides), in tissue homogenates (liver, intestine and kidney), and in the serum.