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The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells. | LitMetric

The sulfite molecule enhances homocysteine toxicity in SH-SY5Y cells.

Mol Biol Rep

Department of Physiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey.

Published: August 2019

AI Article Synopsis

  • Homocysteine (hcy) and sulfite (sft) are investigated for their neurotoxic effects and their role in oxidative stress using SH-SY5Y cells as a model.
  • The study found that the highest toxicity occurred when hcy and sft were combined, causing significant DNA damage and oxidative stress compared to individual treatments.
  • Understanding the impacts of elevated hcy and sft levels may help in delaying the onset of neurodegenerative diseases before symptoms are present.

Article Abstract

Homocysteine (hcy) is an amino acid that contains sulfur species. In healthy individuals, plasma hcy levels are low. The aim of this study was to investigate the potential neurotoxic effects of hcy and sulfite (sft) molecules alone and in their combination, and also to identify the relationship of these substances on oxidative stress. SH-SY5Y cells were used as an invitro neurodegenerative disease model. The SH-SY5Y cells were treated with various concentrations of hcy alone, sft alone (final concentrations in the well were 10-250 µM and 0.1-5 mM, respectively) and a combination of both (hcy + sft). Their cytotoxicity and genotoxic effects were investigated using the XTT test and Comet assay and, their impact on oxidative stress was examined using total antioxidant-oxidant status (TAS-TOS) kits. The highest toxic doses of hcy and sft were found to be 250 μM and 5 mM, respectively, but the maximum toxic effect was observed for hcy + sft (p < 0.001). In addition, an increase in DNA damage was evident in all groups, but maximal damage was inflicted using in hcy + sft (p < 0.001). The oxidative stress index was significantly increased in hcy + sft (p < 0.05). Determining the increase in sft and hcy levels may contribute to delaying the occurrence of diseases before symptoms of neurodegenerative disease appear.

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Source
http://dx.doi.org/10.1007/s11033-019-04850-3DOI Listing

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