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Dichloroacetate Decreases Cell Health and Activates Oxidative Stress Defense Pathways in Rat Alveolar Type II Pneumocytes.

Valauri-Orton A, Bschorer F, Bernd KK - Biomed Res Int (2015)

Bottom Line: This study characterizes the effects of the haloacetate on lung cells by exposing rat alveolar type II (L2) cells to 0-24 mM DCA for 6-24 hours.Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway.These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Davidson College, Davidson, NC 28035, USA.

ABSTRACT
Dichloroacetate (DCA) is a water purification byproduct that is known to be hepatotoxic and hepatocarcinogenic and to induce peripheral neuropathy and damage macrophages. This study characterizes the effects of the haloacetate on lung cells by exposing rat alveolar type II (L2) cells to 0-24 mM DCA for 6-24 hours. Increasing DCA concentration and the combination of increasing DCA concentration plus longer exposures decrease measures of cellular health. Length of exposure has no effect on oxidative stress biomarkers, glutathione, SOD, or CAT. Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway. These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.

No MeSH data available.


Related in: MedlinePlus

Effect of DCA treatment regimes on L2 viability. Cells were exposed to 0, 8, 16, and 24 mM DCA for 6, 16, and 24 hours. Viability was determined by MTT assay with the viability 0 mM DCA treatment for the corresponding exposure time defined as 100%. Bars represent mean ± S.D., n = 5-6. ∗ denotes a significant difference between data from that condition and those without ∗ (p < 0.037).
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fig1: Effect of DCA treatment regimes on L2 viability. Cells were exposed to 0, 8, 16, and 24 mM DCA for 6, 16, and 24 hours. Viability was determined by MTT assay with the viability 0 mM DCA treatment for the corresponding exposure time defined as 100%. Bars represent mean ± S.D., n = 5-6. ∗ denotes a significant difference between data from that condition and those without ∗ (p < 0.037).

Mentions: To investigate the effects of DCA on rat alveolar type II (L2) cells, samples were treated with 0–24 mM DCA at the indicated time points and the MTT assay was used to determine percent viability. Both the duration of DCA exposure and the concentration of DCA in the treatment resulted in significant decreases in cell viability (Figure 1). While no length of exposure to 8 mM DCA compromised cell health, exposure to 16 mM or 24 mM DCA for 24 hours induced significant decreases in viability, 22 and 25%, respectively. In addition, statistical analysis revealed a significant interaction effect between the two variables, indicating that the combination of increased duration of exposure and higher DCA concentrations causes a more severe decline in cell health than changes in either variable alone (p < 0.037).


Dichloroacetate Decreases Cell Health and Activates Oxidative Stress Defense Pathways in Rat Alveolar Type II Pneumocytes.

Valauri-Orton A, Bschorer F, Bernd KK - Biomed Res Int (2015)

Effect of DCA treatment regimes on L2 viability. Cells were exposed to 0, 8, 16, and 24 mM DCA for 6, 16, and 24 hours. Viability was determined by MTT assay with the viability 0 mM DCA treatment for the corresponding exposure time defined as 100%. Bars represent mean ± S.D., n = 5-6. ∗ denotes a significant difference between data from that condition and those without ∗ (p < 0.037).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4537706&req=5

fig1: Effect of DCA treatment regimes on L2 viability. Cells were exposed to 0, 8, 16, and 24 mM DCA for 6, 16, and 24 hours. Viability was determined by MTT assay with the viability 0 mM DCA treatment for the corresponding exposure time defined as 100%. Bars represent mean ± S.D., n = 5-6. ∗ denotes a significant difference between data from that condition and those without ∗ (p < 0.037).
Mentions: To investigate the effects of DCA on rat alveolar type II (L2) cells, samples were treated with 0–24 mM DCA at the indicated time points and the MTT assay was used to determine percent viability. Both the duration of DCA exposure and the concentration of DCA in the treatment resulted in significant decreases in cell viability (Figure 1). While no length of exposure to 8 mM DCA compromised cell health, exposure to 16 mM or 24 mM DCA for 24 hours induced significant decreases in viability, 22 and 25%, respectively. In addition, statistical analysis revealed a significant interaction effect between the two variables, indicating that the combination of increased duration of exposure and higher DCA concentrations causes a more severe decline in cell health than changes in either variable alone (p < 0.037).

Bottom Line: This study characterizes the effects of the haloacetate on lung cells by exposing rat alveolar type II (L2) cells to 0-24 mM DCA for 6-24 hours.Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway.These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.

View Article: PubMed Central - PubMed

Affiliation: Biology Department, Davidson College, Davidson, NC 28035, USA.

ABSTRACT
Dichloroacetate (DCA) is a water purification byproduct that is known to be hepatotoxic and hepatocarcinogenic and to induce peripheral neuropathy and damage macrophages. This study characterizes the effects of the haloacetate on lung cells by exposing rat alveolar type II (L2) cells to 0-24 mM DCA for 6-24 hours. Increasing DCA concentration and the combination of increasing DCA concentration plus longer exposures decrease measures of cellular health. Length of exposure has no effect on oxidative stress biomarkers, glutathione, SOD, or CAT. Increasing DCA concentration alone does not affect total glutathione or its redox ratio but does increase activity in the SOD/CAT oxidative stress defense pathway. These data suggest that alveolar type II cells rely on SOD and CAT more than glutathione to combat DCA-induced stress.

No MeSH data available.


Related in: MedlinePlus