Oxidative stress‐mediated autophagic cell death participates in the neurotoxic effect on SH‐SY5Y cells induced by excessive iodide

Abstract

Excessive iodide could induce intellectual damage in children, which has attracted broad attention. To investigate the neurotoxic effect of iodide and its mechanism, a human dopaminergic neuroblastoma cell line (SH-SY5Y) was treated with different concentrations of potassium iodide (KI). The results showed that excessive iodide could decrease cell viability, reduce glutathione (GSH) and superoxide dismutase (SOD), and increase the degree of autophagy (by changing the cellular ultrastructure and raising the autophagy-related mRNA and protein expression of LC3, Beclin1, and p62), which were correlated with the immunofluorescence labeling. Furthermore, treatment with the autophagy inhibitor 3-methyladenine (3MA), antioxidant N-acetylcysteine (NAC) and 30 mM KI for 24 h was conducted in the following research. 3MA significantly decreased autophagy-related mRNA and protein expression and improved cell viability, indicating that excess iodide induced autophagic cell death. In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62. In summary, autophagic cell death mediated by oxidative stress may participate in excessive iodide-induced SH-SY5Y cell death.

3‐Methyladenine alleviates excessive iodine‐induced cognitive impairment via suppression of autophagy in rat hippocampus

“…Existing findings have indicated that molecular iodine (I 2 ) treatment enhanced the features of autophagy in human breast cancer cell line (MDA‐MB231) . Simultaneously, our study has shown that exposure to potassium iodide could cause autophagic cell death mediated by oxidative stress in SH‐SY5Y cells . In this regard, oxidative stress and autophagy may play a prominent role in the damage action mechanism of excessive iodine.…”

“…Conversely, as autophagy is often induced under conditions of stress that could also lead to cell death, there is growing evidence proposed on the idea that autophagy can act as a cell death mechanism . Luo et al found that the autophagy pathway is involved in the pathophysiologic responses after traumatic brain injury, and inhibition of this pathway may help attenuate traumatic damage and functional outcome deficits .…”

Transport stress induces pig jejunum tissue oxidative damage and results in autophagy/mitophagy activation

“…Many stimuli could induce autophagy, including nutrient starvation, mitochondrial toxins and oxidative stress (Sharma, Pandey, & Saluja, ). Recent research reported that excessive iodide could activate oxidative stress and decrease glutathione (GSH) and SOD levels, leading to increase the degree of autophagy by raising the autophagy‐related mRNA and protein expression of LC3 and beclin‐1 (Cao et al, ; Liu et al, ). Nutrient deficiency at birth can generate oxidative responses in the ovaries causing increased apoptosis and autophagy in both the somatic cells and oocyte (Wang et al, ).…”