Inorganic mercury prevents the differentiation of SH-SY5Y cells: Amyloid precursor protein, microtubule associated proteins and ROS as potential targets

Chin-Chan, Miguel; Bautista, Elizabeth; Alvarado-Cruz, Isabel; Quintanilla‐Vega, Betzabet; Segovia, José

doi:10.1016/j.jtemb.2017.02.002

Cited by 26 publications

(10 citation statements)

References 61 publications

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“…Hg presents toxic effects in the CNS, resulting in changes in neurotransmission [ 34 ], deficiencies in neuronal differentiation [ 35 ], damage to cellular DNA [ 36 , 37 ], changes in the cytoskeleton [ 35 ], variations in intracellular Ca 2+ concentrations [ 38 ], and the production of reactive oxygen species (ROS) by configuring the mechanism of oxidative stress [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Hippocampal Dysfunction Provoked by Mercury Chloride Exposure: Evaluation of Cognitive Impairment, Oxidative Stress, Tissue Injury and Nature of Cell Death

Aragão

Teixeira

Fagundes

et al. 2018

Oxidative Medicine and Cellular Longevity

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Mercury (Hg) is a highly toxic metal, which can be found in its inorganic form in the environment. This form presents lower liposolubility and lower absorption in the body. In order to elucidate the possible toxicity of inorganic Hg in the hippocampus, we investigated the potential of low doses of mercury chloride (HgCl2) to promote hippocampal dysfunction by employing a chronic exposure model. For this, 56 rats were exposed to HgCl2 (0.375 mg/kg/day) via the oral route for 45 days. After the exposure period, the animals were submitted to the cognitive test of fear memory. The hippocampus was collected for the measurement of total Hg levels, analysis of oxidative stress, and evaluation of cytotoxicity, apoptosis, and tissue injury. It was observed that chronic exposure to inorganic Hg promotes an increase in mercury levels in this region and damage to short- and long-term memory. Furthermore, we found that this exposure model provoked oxidative stress, which led to cytotoxicity and cell death by apoptosis, affecting astrocytes and neurons in the hippocampus. Our study demonstrated that inorganic Hg, even with its low liposolubility, is able to produce deleterious effects in the central nervous system, resulting in cognitive impairment and hippocampal damage when administered for a long time at low doses in rats.

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Section: Discussionmentioning

confidence: 99%

Hippocampal Dysfunction Provoked by Mercury Chloride Exposure: Evaluation of Cognitive Impairment, Oxidative Stress, Tissue Injury and Nature of Cell Death

Aragão

Teixeira

Fagundes

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Mercury exposure has been shown to promote the increased accumulation of extracellular Aβ deposits in an in cell model [ 87 ]. A recent study, however, showed that treatment of an in cell model with mercury led to decreased levels of APP, possibly resulting in reduced accumulation of Aβ deposits [ 88 ]. In vitro studies have also demonstrated that mercury is involved in promoting the aggregation of the tau protein [ 87 , 89 ].…”

Section: Environmental Metal Ionsmentioning

confidence: 99%

Metal Ion Effects on Aβ and Tau Aggregation

Kim

Lim

Kim

2018

IJMS

134

153

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Amyloid and tau aggregation are implicated in manifold neurodegenerative diseases and serve as two signature pathological hallmarks in Alzheimer’s disease (AD). Though aging is considered as a prominent risk factor for AD pathogenesis, substantial evidence suggests that an imbalance of essential biometal ions in the body and exposure to certain metal ions in the environment can potentially induce alterations to AD pathology. Despite their physiological importance in various intracellular processes, biometal ions, when present in excessive or deficient amounts, can serve as a mediating factor for neurotoxicity. Recent studies have also demonstrated the contribution of metal ions found in the environment on mediating AD pathogenesis. In this regard, the neuropathological features associated with biometal ion dyshomeostasis and environmental metal ion exposure have prompted widespread interest by multiple research groups. In this review, we discuss and elaborate on findings from previous studies detailing the possible role of both endogenous and exogenous metal ions specifically on amyloid and tau pathology in AD.

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“…Epidemiologically, environmental neurotoxins, such as pesticides, MPP + , 6-hydroxydopamine, rotenone, 3-nitropropionic acid and paraquat, induced neurotoxicity via triggering mitochondrial oxidative stress burdens [1][2][3][4][5] . Levels of ROS exceed the antioxidant capacity of the mitochondria of neurons.…”

Section: Discussionmentioning

confidence: 99%

“…Reactive oxygen species (ROS), especially the free radicals, are implicated in the toxic mechanism of neurotoxins, including rotenone [1][2][3] , lipopolysaccharide [4] and 1-methyl-4-phenylpyridinium (MPP + ) [5] , etc. Mitochondria are key cell organelles that control many processes by maintaining energy production.…”

mentioning

confidence: 99%

S-methyl-L-cysteine Protects against Antimycin A-induced Mitochondrial Dysfunction in Neural Cells via Mimicking Endogenous Methionine-centered Redox Cycle

Guan

Chen

et al. 2020

CURR MED SCI

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SummaryMitochondrial superoxide overproduction is believed to be responsible for the neurotoxicity associated with neurodegeneration. Mitochondria-targeted antioxidants, such as MitoQ, have emerged as potentially effective antioxidant therapies. Methionine sulfoxide reductase A (MsrA) is a key mitochondrial-localized endogenous antioxidative enzyme and it can scavenge oxidizing species by catalyzing the methionine (Met)-centered redox cycle (MCRC). In this study, we observed that the natural L-Met acted as a good scavenger for antimycin A-induced mitochondrial superoxide overproduction in PC12 cells. This antioxidation was largely dependent on the Met oxidase activity of MsrA. S-methyl-L-cysteine (SMLC), a natural analogue of Met that is abundantly found in garlic and cabbage, could activate the Met oxidase activity of MsrA to scavenge free radicals. Furthermore, SMLC protected against antimycin A-induced mitochondrial membrane depolarization and alleviated 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity. Thus, our data highlighted the possibility for SMLC supplement in the detoxication of mitochondrial damage by activating the Met oxidase activity of MsrA.

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Inorganic mercury prevents the differentiation of SH-SY5Y cells: Amyloid precursor protein, microtubule associated proteins and ROS as potential targets

Cited by 26 publications

References 61 publications

Hippocampal Dysfunction Provoked by Mercury Chloride Exposure: Evaluation of Cognitive Impairment, Oxidative Stress, Tissue Injury and Nature of Cell Death

Hippocampal Dysfunction Provoked by Mercury Chloride Exposure: Evaluation of Cognitive Impairment, Oxidative Stress, Tissue Injury and Nature of Cell Death

Metal Ion Effects on Aβ and Tau Aggregation

S-methyl-L-cysteine Protects against Antimycin A-induced Mitochondrial Dysfunction in Neural Cells via Mimicking Endogenous Methionine-centered Redox Cycle

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