[Demonstration of estrogen receptors in perianal tumors in dogs].
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Adenoma↗
Biomedical subjects
F R Ungemach
Publications and source records attributed to F R Ungemach.
Uptake of thymidine into isolated rat hepatocytes. Evidence for two transport systems.
Thymidine transport was studied in isolated rat hepatocytes. In these cells no phosphorylation of the substrate by thymidine kinase occurred subsequent to transport. Results from studies of the concentration-dependent uptake of thymidine indicated two transport systems with about 80-fold differences in their kinetic constants. These systems were denoted as high affinity [Km = 5.3 micron, V = 0.47 pmol/(10(6) cells X s)] and low affinity systems [Km = 480 micron, V = 37.6 pmol/(10(6) cells X s)]. From intracellular to extracellular distribution ratios of [3H]thymidine it could be concluded that the uptake by the high affinity system was a concentrative process while the transport by the low affinity system was non-concentrative. The uptake of [3H]-thymidine by the high affinity system could only be inhibited by unlabeled thymidine. In contrast, all other nucleosides tested (uridine, 2'-deoxycytidine, and 2'-deoxyguanosine) were equally effective in inhibiting the low affinity system competitively. The results would suggest that in hepatocytes lacking phosphorylation by thymidine kinase, thymidine is taken up by a high and a low affinity system working in tandem. The high affinity system seems to be an active transport process with narrow substrate specificity. Thymidine uptake by the low affinity system is a facilitated diffusion process. This system is considered to be a common transport route for nucleosides of different structures.
Animals↗
Pathobiochemical mechanisms of hepatocellular damage following lipid peroxidation.
In hepatocytes, cytotoxic events induced by haloalkanes or acute iron-overload exhibit neither a quantitative nor a temporal correlation to lipid peroxidation or covalent binding. Thus, secondary pathological mechanisms have been postulated linking initial focal reactions of free radicals and end stage pathological consequences. Due to the crucial role of plasma-membrane integrity in the cytotoxic process it has to be supposed that relevant secondary pathological mechanisms finally impair the physico-chemical and functional properties of this membrane. Based on recent developments a chain of causality is proposed as a two-step activation of phospholipase A2 producing cytolytic amounts of lysophosphatides. In this cascade, the initial activating step is a decrease of membrane lipid fluidity induced by lipid peroxidation and/or by calcium binding and intramembranous formation of 4-hydroxynonenal. This enzyme activation is further amplified by the early rise of cytosolic calcium. Consequently, increasing amounts of lysophosphatides progressively impair membrane configuration thus improving the substrate accessibility for phospholipase A2 in a second activation step. Finally, the lysophosphatides reach plasma membrane-lytic concentrations by this autocatalytic enzyme activation.
Animals↗
Effect of local anesthetics on cellular respiration and thymidine transport in hepatocytes from young and old rats.
The effect of local anesthetics (procaine, nicotinoyl-procaine, tetracaine, and dibucaine) on thymidine uptake and cellular respiration was investigated in hepatocytes from 3- and 24-month-old rats. All local anesthetics inhibited the "high-affinity" as well as the "low-affinity" thymidine transport system in a non-competitive manner immediately upon addition. Nicotinoyl-procaine, tetracaine, and dibucaine showed a similar inhibition profile with an inhibition of 10--15% at 50 mumol/l, or of more than 60% at 1 mmol/l. The less-lipophilic procaine showed a distinctly lower inhibition (10% at 1 mmol/l). The inhibitory effect was reversible and not dependent on Ca2+. All local anesthetics exerted identical effects in hepatocytes from young and old rats. Nicotinoyl-procaine and tetracaine inhibited cellular respiration in young and old rats up to a maximum of 50%. Procaine did not reduce O2 consumption below 1 mmol/l. This inhibition appeared also immediately upon addition, was not reversible, and not dependent on Ca2+. It is concluded that local anesthetics impair quite different biological processes like thymidine transport and cellular respiration in hepatocytes from young and old animals even at concentrations below 100 mumol/l. The magnitude of inhibition was correlated to the lipid solubility of the local anesthetics. The mechanism seemed to be different to the anesthetic action and it is supposed that it is a direct hydrophobic interaction with membrane proteins. Thus the local anesthetic-induced increase in membrane fluidity could not improve the age-dependent impairment of thymidine transport. The reduction of respiration is considered to be due to reduced O2 diffusion. This inhibition is in striking contrast to previously observed stimulatory effects which in part lead to the use of local anesthetics in geriatrics.
Aging↗