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Lycopene Pretreatment Ameliorates Acute Ethanol Induced NAD(+) Depletion in Human Astroglial Cells.

Guest J, Guillemin GJ, Heng B, Grant R - Oxid Med Cell Longev (2015)

Bottom Line: Excessive alcohol consumption is associated with reduced brain volume and cognition.While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes.Unexpectedly, in U251 cells lycopene treatment at concentrations ≥ 5 μM resulted in significant reductions in [NAD(H)].

View Article: PubMed Central - PubMed

Affiliation: Australasian Research Institute, Sydney Adventist Hospital, Sydney, NSW 2076, Australia ; Department of Pharmacology, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia.

ABSTRACT
Excessive alcohol consumption is associated with reduced brain volume and cognition. While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes. In order to further characterise the effect of acute ethanol exposure on oxidative damage and NAD(+) levels in the brain, human U251 astroglioma cells were exposed to physiologically relevant doses of ethanol (11 mM, 22 mM, 65 mM, and 100 mM) for ≤ 30 minutes. Ethanol exposure resulted in a dose dependent increase in both ROS and poly(ADP-ribose) polymer production. Significant decreases in total NAD(H) and sirtuin 1 activity were also observed at concentrations ≥ 22 mM. Similar to U251 cells, exposure to ethanol (≥22 mM) decreased levels of NAD(H) in primary human astrocytes. NAD(H) depletion in primary astrocytes was prevented by pretreatment with 1 μM of lycopene for 3.5 hours. Unexpectedly, in U251 cells lycopene treatment at concentrations ≥ 5 μM resulted in significant reductions in [NAD(H)]. This study suggests that exposure of the brain to alcohol at commonly observed blood concentrations may cause transitory oxidative damage which may be at least partly ameliorated by lycopene.

No MeSH data available.


Related in: MedlinePlus

Ethanol exposure of U251 cells for ≤ 30 minutes, effects on (a) reactive oxygen species production, (b) generation of poly(ADP-ribose) polymers, (c) NAD(H) concentration, and (d) SIRT1 activity. ∗∗P < 0.01, ∗∗∗P < 0.001. Data are presented as mean ± SEM.
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fig1: Ethanol exposure of U251 cells for ≤ 30 minutes, effects on (a) reactive oxygen species production, (b) generation of poly(ADP-ribose) polymers, (c) NAD(H) concentration, and (d) SIRT1 activity. ∗∗P < 0.01, ∗∗∗P < 0.001. Data are presented as mean ± SEM.

Mentions: Exposure to 11 mM, 22 mM, 65 mM (P < 0.01), and 100 mM (P < 0.001) of ethanol for 10 minutes increased intracellular ROS production above control by 7.9 ± 3.9%, 11.5 ± 4.1%, 16.6 ± 3.6%, and 26.7 ± 5.8%, respectively; however statistically significant differences were only observed following exposure to 65 mM and 100 mM of ethanol (Figure 1(a)).


Lycopene Pretreatment Ameliorates Acute Ethanol Induced NAD(+) Depletion in Human Astroglial Cells.

Guest J, Guillemin GJ, Heng B, Grant R - Oxid Med Cell Longev (2015)

Ethanol exposure of U251 cells for ≤ 30 minutes, effects on (a) reactive oxygen species production, (b) generation of poly(ADP-ribose) polymers, (c) NAD(H) concentration, and (d) SIRT1 activity. ∗∗P < 0.01, ∗∗∗P < 0.001. Data are presented as mean ± SEM.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4446500&req=5

fig1: Ethanol exposure of U251 cells for ≤ 30 minutes, effects on (a) reactive oxygen species production, (b) generation of poly(ADP-ribose) polymers, (c) NAD(H) concentration, and (d) SIRT1 activity. ∗∗P < 0.01, ∗∗∗P < 0.001. Data are presented as mean ± SEM.
Mentions: Exposure to 11 mM, 22 mM, 65 mM (P < 0.01), and 100 mM (P < 0.001) of ethanol for 10 minutes increased intracellular ROS production above control by 7.9 ± 3.9%, 11.5 ± 4.1%, 16.6 ± 3.6%, and 26.7 ± 5.8%, respectively; however statistically significant differences were only observed following exposure to 65 mM and 100 mM of ethanol (Figure 1(a)).

Bottom Line: Excessive alcohol consumption is associated with reduced brain volume and cognition.While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes.Unexpectedly, in U251 cells lycopene treatment at concentrations ≥ 5 μM resulted in significant reductions in [NAD(H)].

View Article: PubMed Central - PubMed

Affiliation: Australasian Research Institute, Sydney Adventist Hospital, Sydney, NSW 2076, Australia ; Department of Pharmacology, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia.

ABSTRACT
Excessive alcohol consumption is associated with reduced brain volume and cognition. While the mechanisms by which ethanol induces these deleterious effects in vivo are varied most are associated with increased inflammatory and oxidative processes. In order to further characterise the effect of acute ethanol exposure on oxidative damage and NAD(+) levels in the brain, human U251 astroglioma cells were exposed to physiologically relevant doses of ethanol (11 mM, 22 mM, 65 mM, and 100 mM) for ≤ 30 minutes. Ethanol exposure resulted in a dose dependent increase in both ROS and poly(ADP-ribose) polymer production. Significant decreases in total NAD(H) and sirtuin 1 activity were also observed at concentrations ≥ 22 mM. Similar to U251 cells, exposure to ethanol (≥22 mM) decreased levels of NAD(H) in primary human astrocytes. NAD(H) depletion in primary astrocytes was prevented by pretreatment with 1 μM of lycopene for 3.5 hours. Unexpectedly, in U251 cells lycopene treatment at concentrations ≥ 5 μM resulted in significant reductions in [NAD(H)]. This study suggests that exposure of the brain to alcohol at commonly observed blood concentrations may cause transitory oxidative damage which may be at least partly ameliorated by lycopene.

No MeSH data available.


Related in: MedlinePlus