Carbon starvation of Salmonella typhimurium does not cause a general increase of mutation rates.

Mutation rates in bacteria can vary depending on the genetic target studied and the specific growth conditions of the cells. Here, two different methods were used to determine how rates of mutation to antibiotic resistance, auxotrophy, and prototrophy were influenced by carbon starvation on agar plates. The rate of mutation to rifampin resistance was increased by starvation as measured by fluctuation tests, similar to what has been reported previously for Escherichia coli. In contrast, the rates of mutation to various types of auxotrophy were unaffected or decreased as measured by both fluctuation tests and a repeated-streaking procedure. Similarly, the rates of reversion to prototrophy of his and lac nonsense and missense mutations were unaffected by starvation. Thus, mutation rates of different genetic targets can be affected differently by starvation and we conclude that carbon starvation is not generally mutagenic in Salmonella typhimurium.

SAM prevents impairment of glucose-stimulated insulin secretion caused by hexose deprivation or starvation.

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. Three models were now used to investigate whether SAM protects the B-cell against the impairment of glucose-stimulated insulin release caused by either glucose deprivation or starvation. In the first model, preincubation of the islets for 180 min at low glucose concentration in the presence of SAM prevented the decrease in the secretory response to D-glucose otherwise observed during a subsequent incubation. In the second model, an impaired secretory response to D-glucose was observed after 3-day culture at low (2.8 or 5.6 mM) as distinct from high (11.1 mM) hexose concentration and the presence of SAM in the culture medium again protected against this anomaly. In the third model, the infusion of SAM for 3 days to starved rats restored the secretory potential of isolated islets to a level comparable to that otherwise found in fed rats. Thus, during glucose deprivation or starvation, SAM is indeed able to maintain B-cell responsiveness to D-glucose.

Studies on the mechanism of lymphocyte-mediated cytolysis. V. The use of cytochalasins A and B to dissociate glucose transport from the lytic event.

The lysis of DBA/2 mastocytoma cells (P815) by alloimmune C57BL/6 thymus-derived lymphocytes was inhibited by cytochalasin A (CA) and cytochalasin B (CB). Although CB prevented incorporation of glucose into lymphocytes, the effector cell susceptibility to the drug was independent of the hexose content of the culture medium. Indeed, cytolysis occurred in the absence of exogenous hexose. Futhermore CA which, like CB, inhibited the adsorption of effector spleen cell populations onto homologous allogeneic monolyers and prevented the migratory movement of lymphoid cells did so without affecting incorporation of glucose into lymphocytes. These findings suggest that the inhibition of cytolysis by CA and CB is mediated by common inhibitory effects on membrane mobility rather than by affecting glucose uptake.