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Melatonin protects SK‐N‐SH neuroblastoma cells from amphetamine‐induced neurotoxicity
Author(s) -
Klongpanichapak Sirirat,
PhansuwanPujito Pansiri,
Ebadi Manuchair,
Govitrapong Piyarat
Publication year - 2007
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2007.00444.x
Subject(s) - melatonin , amphetamine , neurotoxicity , pharmacology , melatonin receptor , medicine , neuroblastoma , chemistry , endocrinology , toxicity , biology , cell culture , dopamine , genetics
Several hypotheses regarding the mechanism underlying amphetamine‐induced neurotoxicity have been proposed. One of them is based on the observation of free radical formation and oxidative stress produced by auto‐oxidation of dopamine (DA). The formation of DA‐related reactive oxygen species (ROS) such as superoxide and hydroxyl radicals appears to play an important role in amphetamine‐induced neurotoxicity. Melatonin, the main secretory product of pineal gland, is well known for its protective effects that are currently attributed mainly to its radical scavenging and antioxidant properties. The present study was conducted to investigate the protective effects of melatonin on d ‐amphetamine (AMPH)‐induced neurotoxicity in cultured human dopaminergic neuroblastoma SK‐N‐SH cells. Our data indicate that AMPH significantly reduces cell viability, induces oxidative stress (enhances ROS production and malondialdehyde levels), up‐regulates α ‐synuclein expression and decreases intracellular ATP levels. However, pretreatment of SK‐N‐SH cells with melatonin prevents AMPH‐induced loss of cell viability and induction of oxidative stress, while reducing α ‐synuclein expression and increasing ATP production. These results suggest that the antioxidant properties of melatonin may provide a protective mechanism against AMPH‐induced neuronal degeneration.