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Melatonin Attenuates Oxidative Damage Induced by Acrylamide In Vitro and In Vivo.

Pan X, Zhu L, Lu H, Wang D, Lu Q, Yan H - Oxid Med Cell Longev (2015)

Bottom Line: Results in cells showed that reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after ACR treatment for 24 h.Using MDA generation, glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in rat cerebellum as indicators, MT alleviated ACR-induced lipid peroxidation and depressed antioxidant capacity.Our results suggest that MT effectively prevents oxidative damage induced by ACR.

View Article: PubMed Central - PubMed

Affiliation: Department of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; Institute for Environmental Medicine, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

ABSTRACT
Acrylamide (ACR) has been classified as a neurotoxic agent in animals and humans. Melatonin (MT) has been shown to be potentially effective in preventing oxidative stress related neurodegenerative disorders. In this study, whether MT exerted a protective effect against ACR-induced oxidative damage was investigated. Results in cells showed that reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after ACR treatment for 24 h. MT preconditioning or cotreatment with ACR reduced ROS and MDA products, whereas the inhibitory effect of MT on oxidant generation was attenuated by blocking the MT receptor. Increased DNA fragmentation caused by ACR was significantly decreased by MT coadministration. In vivo, rats at 40 mg/kg/day ACR by gavage for 12 days showed weight loss and gait abnormality, Purkinje cell nuclear condensation, and DNA damage in rat cerebellum. MT (i.p) cotreatment with ACR not only recovered weight and gait of rats, but also decreased nuclear condensation and DNA damage in rat cerebellum. Using MDA generation, glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in rat cerebellum as indicators, MT alleviated ACR-induced lipid peroxidation and depressed antioxidant capacity. Our results suggest that MT effectively prevents oxidative damage induced by ACR.

No MeSH data available.


Related in: MedlinePlus

Effects of MT on ROS and MDA generations induced by ACR in PC12 cells. Intracellular ROS was evaluated by DCFH-DA detection. Fluorescent photographs were shown after exposure to ACR with or without MT cotreatment for 24 h (scale bar: 25 μm) (a). In addition, ROS (b) and MDA (d) productions induced by treatment with ACR (1.25, 2.5, and 5 mM) alone for 1, 3, 6, 12, and 24 h. Moreover, MT (50 μM) and luzindole (0.2 μM) interventions at different times: 24 h pretreatment, simultaneously, and 3 h posttreatment with ACR (2.5 mM) for 6 h were designed ((c) and (e)). The results are expressed as the mean ± SD (n = 8). ∗P < 0.05, ∗∗P < 0.01 versus the vehicle control group. #P < 0.05, ##P < 0.01 versus the ACR treatment group, &P < 0.05, &&P < 0.01 versus the ACR + MT cotreatment group.
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fig4: Effects of MT on ROS and MDA generations induced by ACR in PC12 cells. Intracellular ROS was evaluated by DCFH-DA detection. Fluorescent photographs were shown after exposure to ACR with or without MT cotreatment for 24 h (scale bar: 25 μm) (a). In addition, ROS (b) and MDA (d) productions induced by treatment with ACR (1.25, 2.5, and 5 mM) alone for 1, 3, 6, 12, and 24 h. Moreover, MT (50 μM) and luzindole (0.2 μM) interventions at different times: 24 h pretreatment, simultaneously, and 3 h posttreatment with ACR (2.5 mM) for 6 h were designed ((c) and (e)). The results are expressed as the mean ± SD (n = 8). ∗P < 0.05, ∗∗P < 0.01 versus the vehicle control group. #P < 0.05, ##P < 0.01 versus the ACR treatment group, &P < 0.05, &&P < 0.01 versus the ACR + MT cotreatment group.

Mentions: To observe the effect of MT on oxidative stress induced by ACR, ROS accumulation and MDA generation in PC12 cells were determined. ACR exposure significantly enhanced the fluorescent intensity compared with vehicle controls in PC12 cells (Figure 4(a)). The significant increases in ROS generation were found in the 1.25 mmol/L ACR treatment group at 3 h, but in the 2.5 and 5 mmol/L ACR treatment groups at 1 h (Figure 4(b)). ROS levels increased in PC12 cells with ACR treatment in a concentration- and time-dependent manner. MT at 50 μmol/L pre-24 h treatment with ACR, as well as cotreatment with ACR, protected cells from ROS accumulation induced by ACR (Figure 4(c)). MDA content at 5 mmol/L ACR treatment for 3, 6, 12, and 24 h increased significantly (Figure 4(d)). When culture cells were pretreated with MT for 24 h, ACR treatment for 24 h significantly decreased the MDA content (Figure 4(e)). Similarly, the protective effect of MT on ACR-induced ROS and MDA generation was inhibited by 0.2 μmol/L luzindole pretreatment for 24 h.


Melatonin Attenuates Oxidative Damage Induced by Acrylamide In Vitro and In Vivo.

Pan X, Zhu L, Lu H, Wang D, Lu Q, Yan H - Oxid Med Cell Longev (2015)

Effects of MT on ROS and MDA generations induced by ACR in PC12 cells. Intracellular ROS was evaluated by DCFH-DA detection. Fluorescent photographs were shown after exposure to ACR with or without MT cotreatment for 24 h (scale bar: 25 μm) (a). In addition, ROS (b) and MDA (d) productions induced by treatment with ACR (1.25, 2.5, and 5 mM) alone for 1, 3, 6, 12, and 24 h. Moreover, MT (50 μM) and luzindole (0.2 μM) interventions at different times: 24 h pretreatment, simultaneously, and 3 h posttreatment with ACR (2.5 mM) for 6 h were designed ((c) and (e)). The results are expressed as the mean ± SD (n = 8). ∗P < 0.05, ∗∗P < 0.01 versus the vehicle control group. #P < 0.05, ##P < 0.01 versus the ACR treatment group, &P < 0.05, &&P < 0.01 versus the ACR + MT cotreatment group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4491391&req=5

fig4: Effects of MT on ROS and MDA generations induced by ACR in PC12 cells. Intracellular ROS was evaluated by DCFH-DA detection. Fluorescent photographs were shown after exposure to ACR with or without MT cotreatment for 24 h (scale bar: 25 μm) (a). In addition, ROS (b) and MDA (d) productions induced by treatment with ACR (1.25, 2.5, and 5 mM) alone for 1, 3, 6, 12, and 24 h. Moreover, MT (50 μM) and luzindole (0.2 μM) interventions at different times: 24 h pretreatment, simultaneously, and 3 h posttreatment with ACR (2.5 mM) for 6 h were designed ((c) and (e)). The results are expressed as the mean ± SD (n = 8). ∗P < 0.05, ∗∗P < 0.01 versus the vehicle control group. #P < 0.05, ##P < 0.01 versus the ACR treatment group, &P < 0.05, &&P < 0.01 versus the ACR + MT cotreatment group.
Mentions: To observe the effect of MT on oxidative stress induced by ACR, ROS accumulation and MDA generation in PC12 cells were determined. ACR exposure significantly enhanced the fluorescent intensity compared with vehicle controls in PC12 cells (Figure 4(a)). The significant increases in ROS generation were found in the 1.25 mmol/L ACR treatment group at 3 h, but in the 2.5 and 5 mmol/L ACR treatment groups at 1 h (Figure 4(b)). ROS levels increased in PC12 cells with ACR treatment in a concentration- and time-dependent manner. MT at 50 μmol/L pre-24 h treatment with ACR, as well as cotreatment with ACR, protected cells from ROS accumulation induced by ACR (Figure 4(c)). MDA content at 5 mmol/L ACR treatment for 3, 6, 12, and 24 h increased significantly (Figure 4(d)). When culture cells were pretreated with MT for 24 h, ACR treatment for 24 h significantly decreased the MDA content (Figure 4(e)). Similarly, the protective effect of MT on ACR-induced ROS and MDA generation was inhibited by 0.2 μmol/L luzindole pretreatment for 24 h.

Bottom Line: Results in cells showed that reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after ACR treatment for 24 h.Using MDA generation, glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in rat cerebellum as indicators, MT alleviated ACR-induced lipid peroxidation and depressed antioxidant capacity.Our results suggest that MT effectively prevents oxidative damage induced by ACR.

View Article: PubMed Central - PubMed

Affiliation: Department of Health Toxicology, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China ; Institute for Environmental Medicine, MOE Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

ABSTRACT
Acrylamide (ACR) has been classified as a neurotoxic agent in animals and humans. Melatonin (MT) has been shown to be potentially effective in preventing oxidative stress related neurodegenerative disorders. In this study, whether MT exerted a protective effect against ACR-induced oxidative damage was investigated. Results in cells showed that reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after ACR treatment for 24 h. MT preconditioning or cotreatment with ACR reduced ROS and MDA products, whereas the inhibitory effect of MT on oxidant generation was attenuated by blocking the MT receptor. Increased DNA fragmentation caused by ACR was significantly decreased by MT coadministration. In vivo, rats at 40 mg/kg/day ACR by gavage for 12 days showed weight loss and gait abnormality, Purkinje cell nuclear condensation, and DNA damage in rat cerebellum. MT (i.p) cotreatment with ACR not only recovered weight and gait of rats, but also decreased nuclear condensation and DNA damage in rat cerebellum. Using MDA generation, glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in rat cerebellum as indicators, MT alleviated ACR-induced lipid peroxidation and depressed antioxidant capacity. Our results suggest that MT effectively prevents oxidative damage induced by ACR.

No MeSH data available.


Related in: MedlinePlus