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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 on L2 cell SOD activity. Cells were exposed to DCA at concentrations of 0, 8, 16, and 24 mM. SOD activity at 8, 16, and 24 hr DCA exposure was pooled and that average value normalized to baseline SOD levels (0 mM DCA) and mean ± S.D. is shown. n = 33–36. Columns with no shared superscripts are significantly different (p < 0.003).
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fig3: Effect of DCA on L2 cell SOD activity. Cells were exposed to DCA at concentrations of 0, 8, 16, and 24 mM. SOD activity at 8, 16, and 24 hr DCA exposure was pooled and that average value normalized to baseline SOD levels (0 mM DCA) and mean ± S.D. is shown. n = 33–36. Columns with no shared superscripts are significantly different (p < 0.003).

Mentions: Superoxide dismutase (SOD) and catalase (CAT) function in an antioxidant pathway that detoxifies superoxide anion to molecular oxygen and water. The duration of exposure to DCA (0–24 hr) did not have an effect on this metric and no duration: concentration interaction effect was seen. However, SOD activity increases as the DCA treatment concentration rises (Figure 3). Treatment of L2 cells with DCA concentrations of 16 mM and 24 mM resulted in the increase of SOD activity by 9 and 11%, respectively, over the corresponding control (p < 0.0003).


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 on L2 cell SOD activity. Cells were exposed to DCA at concentrations of 0, 8, 16, and 24 mM. SOD activity at 8, 16, and 24 hr DCA exposure was pooled and that average value normalized to baseline SOD levels (0 mM DCA) and mean ± S.D. is shown. n = 33–36. Columns with no shared superscripts are significantly different (p < 0.003).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4537706&req=5

fig3: Effect of DCA on L2 cell SOD activity. Cells were exposed to DCA at concentrations of 0, 8, 16, and 24 mM. SOD activity at 8, 16, and 24 hr DCA exposure was pooled and that average value normalized to baseline SOD levels (0 mM DCA) and mean ± S.D. is shown. n = 33–36. Columns with no shared superscripts are significantly different (p < 0.003).
Mentions: Superoxide dismutase (SOD) and catalase (CAT) function in an antioxidant pathway that detoxifies superoxide anion to molecular oxygen and water. The duration of exposure to DCA (0–24 hr) did not have an effect on this metric and no duration: concentration interaction effect was seen. However, SOD activity increases as the DCA treatment concentration rises (Figure 3). Treatment of L2 cells with DCA concentrations of 16 mM and 24 mM resulted in the increase of SOD activity by 9 and 11%, respectively, over the corresponding control (p < 0.0003).

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