Influence of beta-adrenergic antagonists on cell proliferation rates in the kidney of untreated and diethylnitrosamine-treated male F344 rats.

Some nongenotoxic chemicals which cause kidney tumors have been shown to stimulate tubular cell proliferation. The aim of this study was to evaluate the effects of two beta-adrenoreceptor blocking agents, propranolol and atenolol, on cell proliferation rates in the kidneys of male F344 rats. Immunohistochemical expression of proliferating cell nuclear antigen (PCNA) and mitotic index have been examined in formalin-stored kidneys from F344 rats used in an initiation-promotion study of carcinogenesis.

Effect of tumor-promoting and anti-promoting chemicals on the viability and junctional coupling of human HeLa cells transfected with DNAs coding for various murine connexin proteins.

Gap-junctional intercellular communication is thought to be essential for maintaining cellular homeostasis and growth control. Its perturbation entails toxicological implications and it has been correlated with the in vivo tumor-promoting potential of chemicals. Little is known about the mechanism(s) responsible for the tumor promoters interference with the cellular coupling.

Evaluation of the tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, in liver of Fischer 344 rats.

The tumor-promoting activity of two beta-adrenoreceptor blocking agents, propranolol and atenolol, was tested in a two-stage protocol of hepatocarcinogenesis in male and female Fischer 344 rats. Propranolol is a lipophilic non-selective beta-blocker mainly eliminated via the liver; atenolol is a hydrophilic beta 1-selective blocking agent, mainly eliminated via the kidney. Animals were initiated with a single dose of diethylnitrosamine (DEN, 200 mg/kg, i.

The protective role of high-density lipoprotein on oxidized-low-density-lipoprotein-induced U937/endothelial cell interactions.

The adherence of monocytes to the endothelium is an early event in atherogenesis. We have investigated this process by examining whether native and oxidized low-density and high-density lipoproteins could modulate this process. Only oxidized low-density lipoprotein caused a significant dose-dependent and time-dependent increase in U937 monocyte-like cell line binding to human endothelial cells, by a process which required de novo protein synthesis.

Endogenous interleukin 1 alpha must be transported to the nucleus to exert its activity in human endothelial cells.

We have previously shown that the signal peptideless cytokine interleukin 1 alpha (IL-1 alpha) may play a role as an intracellular regulator of human endothelial cell senescence (J. A. M.