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Biomedical subjects

A K Balin

Publications and source records attributed to A K Balin.

28 records · Page 2Linked to original sources
PubMed1986

Mechanisms of biologic aging.

The authors outline the progression of thought on the mechanism of the aging process, giving emphasis to environmental factors that influence genetic events. Discussion is limited to those theories that explain fundamental causes of aging and have a firm thermodynamic basis. The authors propose that the cumulative result of continual oxidative stress and other thermodynamic processes (such as amino-acid racemization and nonenzymatic glycosylation), resulting in altered function and increasing the net entropy of living systems, governs the rate of the aging process.

Aging↗
PubMed1984

Oxygen modulates growth of human cells at physiologic partial pressures.

We have examined the growth of human diploid fibroblasts (WI-38 and IMR90) as a function of initial seeding density and oxygen tension. Cells at young and mid-passage levels were subcultivated in Dulbecco's modified Eagle's medium with 10% fetal bovine serum at 0.005, 0.01, 0.03, 0.1, 0.3, 1, and 2 X 10(4) cells/cm2. Flasks were equilibrated before and after seeding with 1 of 10 gas mixtures containing the desired oxygen tension (9-591 mm Hg) and placed in incubators that measure and maintain a preset oxygen tension. The partial pressure of oxygen (PO2) in media of all flasks was determined at harvest. Cells were shielded from light of wavelength less than 500 nm. Cell growth varied inversely with oxygen tension and seeding density. At 50 cells/cm2, growth was maximal at PO2 9 and 16 mm Hg. Growth was progressively inhibited as the oxygen tension was increased. The population doubling increase at 14 d was 8.6 for PO2 9 and 16 mm Hg, 5.8 for PO2 42 mm Hg, 3.8 for PO2 78 mm Hg, 3.8 for PO2 104 mm Hg, and 3 for PO2 138 mm Hg. As the seeding density was increased, the differences in growth at PO2 less than 140 mm Hg were progressively minimized, such that at seeding densities of 10(4) cells/cm2 there was little difference in the rate of exponential growth or the final saturation density of cells cultivated between PO2 9 and 96 mm Hg. At all seeding densities tested, growth was progressively inhibited when the PO2 was increased greater than 140 mm Hg. The seeding density dependence of oxygen's influence on cellular growth is not explained by oxygen consumption of higher density cultures. Oxygen acts directly on the cells and not by destroying some essential medium component. We have found that oxygen regulates the growth of human cells under pressures of oxygen physiologic to humans, and that oxygen toxicity contributes to the seeding density dependence of cellular growth commonly seen in cell culture.

Cell Count↗
PubMed1981

Spongiosis.

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Edema↗
PubMed1978

Oxygen-sensitive stages of the cell cycle of human diploid cells.

We had established that growth of human diploid WI-38 cells is reversibly inhibited by elevated partial pressures of oxygen (PO2) and we were interested in determining where in the cell cycle growth was delayed. A technique combining cytospectrophotometry and autoradiography was used to determine cell cycle parameters. Confluent cells that were subcultivated and exposed to a PO2 of 365 +/- 8 mm Hg were delayed primarily after DNA synthesis but before metaphase. At a PO2 of 590 +/- 35 mm Hg, most cells did not initiate DNA synthesis, and the few that did, failed to complete the process. When exponentially growing cells that had already begun DNA synthesis were exposed to a PO2 of 590 p 35 mm Hg, they accumulated after completing DNA synthesis but before initiating mitosis. The rate at which (3H)thymidine was incorporated into DNA was inversely correlated with oxygen tension (PO2 of 135--590 mm Hg). These results suggest that the process most sensitive to oxygen causes cells to be delayed after DNA synthesis but before metaphase. Slightly higher PO2's were needed to inhibit the initiation of DNA synthesis. Further, the rate of DNA synthesis is decreased by elevated oxygen tensions.

Cell Cycle↗
PubMed1977

The effect of oxygen and vitamin E on the lifespan of human diploid cells in vitro.

Human diploid cells (WI-38) were serially subcultivated at partial pressures of oxygen (Po2) ranging from 5.6 mm Hg to 608 mm Hg. At a Po2 of 5.6 mm Hg, the number of doublings to phase out was less than that of control cells at a Po2 of 137 mm Hg. Cultures grown at Po2's of 24, 49, or 137 mm Hg grew at the same rate and phased out after a similar number of population doublings. Population lifespan was markedly shortened by chronic exposure to elevated Po2's, a phenomenon that was, in part, reversible. d-1-alpha-Tocopherol (10 microgram/ml or 100 microgram/ml) homogenized into the medium at each weekly subcultivation did not extend the lifespan of cells at reduced, ambient, or elevated oxygen tensions. These results indicate that neither oxygen toxicity nor free radical reactions play a significant role in limiting the lifespan of WI-38 cells grown in vitro under ambient oxygen tensions (Po2 137 mm Hg).

Cell Division↗
PubMed1976

The effect of oxygen tension on the growth and metabolism of WI-38 cells.

The effect of oxygen tension on cellular growth and metabolism was studied in actively growing WI-38 cells [greater than 90% labeled nuclei (LN)] grown under atmospheres containing 5% CO2 and various combinations of O2 and N2. Cells grown under a partial pressure of oxygen (PO2) of 7.8 +/- 3.5 mm Hg had a significantly slower growth rate, lower saturation densities and higher rates of glucose consumption and lactate production than did cells grown under a PO2 of 44 +/- 7 mm Hg. There were no significant differences in saturation density or the rates of glucose consumption or lactate production between cells grown under PO2 26 +/- 4 mm Hg, 44 +/- 7 mm Hg, or 134 +/- 11 mm Hg. Population doubling time was slightly prolonged at a PO2 of 134 mm Hg compared to a PO2 of 44 mm Hg. Cells grown under a PO2 of 291 +/- 25 mm Hg showed only 20-30% of the growth rate and 10-20% of the saturation density of cells grown under a PO2 of 134 mm Hg. Despite this reduced growth, cells grown under a PO2 of 291 mm Hg consumed four to six times as much glucose and produced four to six times as much lactate per cell as cells grown at a PO2 of 134 mm Hg. Cells grown under a PO2 of 560 +/- 38 mm Hg attached but did not proliferate. This toxic effect of oxygen on cell proliferation was reversible and was not due to an effect of oxygen on the media.

Cell Division↗
PubMed1976

Atmospheric stability in cell culture vessels.

We have investigated that atmospheric stability in polystyrene and glass cell culture vessels by measuring the dissolved O2 and CO2 in the media of both seeded and unseeded culture vessels incubated at 37 degrees C. There was no diffusion of either O2 or CO2 through glass vessels. At low partial pressures of oxygen (PO2), oxygen diffused into the polystyrene flasks at a rate of 1 to 2 mmHg per 24 hr, and at high PO2, oxygen diffused slowly out of polystyrene flasks. CO2 diffused out of polystyrene flasks with a half-time of 260 hr resulting in a considerable elevation in pH. In seeded polystyrene flasks with the PO2 less than or equal to room air, cellular oxygen consumption was masked by the inward diffusion of oxygen. In addition, the fall in pH due to metabolic CO2 and organic acid production during cell growth in polystyrene flasks was buffered by the diffusion of CO2 out of the vessels.

Carbon Dioxide↗
PubMedDate not supplied

Normal replicative lifespan of Alzheimer skin fibroblasts.

Cultured skin fibroblasts from four patients with Alzheimer's disease had life spans comparable to those of six age-sex matched controls, whether measured by passages to phase-out, cumulative population doublings to phase out, or percentage of nuclei incorporating [3H]thymidine (Cristofalo index). These results provide direct experimental evidence that Alzheimer's disease is not simply a form of accelerated aging. They suggest that the abnormalities, described by several groups, in Alzheimer fibroblasts reflect the disease rather than the physiological age of the donor, making the cultured cell a valid tool for studying the cellular pathophysiology of this disorder. Together with other data, these observations raise the possibility that some forms of Alzheimer's disease may represent inborn error(s) of metabolism of late clinical onset.

Aged↗