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Methylmercury and H...
Methylmercury and H2O2 provoke lysosomal damage in human astrocytoma D384 cells followed by apoptosis
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- Daré, Elisabetta (författare)
- The National Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, Stockholm, Sweden
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- Li, Wei, 1962- (författare)
- Linköpings universitet,Institutionen för nervsystem och rörelseorgan,Hälsouniversitetet,Patologi II,Patologi
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- Zhivotovsky, Boris (författare)
- The National Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, Stockholm, Sweden
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- Yuan, Ximing, 1959- (författare)
- Linköpings universitet,Institutionen för nervsystem och rörelseorgan,Hälsouniversitetet,Patologi II
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- Ceccatelli, Sandra (författare)
- The National Institute of Environmental Medicine, Division of Toxicology and Neurotoxicology, Karolinska Institutet, Stockholm, Sweden
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- Yuan, Xi Ming, 1959- (författare)
- Linköpings universitet,Hälsouniversitetet,Patologi
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(creator_code:org_t)
- Linköping : Elsevier, 2001
- 2001
- Engelska.
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Ingår i: Free Radical Biology & Medicine. - Linköping : Elsevier. - 0891-5849 .- 1873-4596. ; 30:12, s. 1347-1356
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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Abstract
Ämnesord
Stäng
- Methylmercury (MeHg) is a neurotoxic agent acting via diverse mechanisms, including oxidative stress. MeHg also induces astrocytic dysfunction, which can contribute to neuronal damage. The cellular effects of MeHg were investigated in human astrocytoma D384 cells, with special reference to the induction of oxidative-stress-related events. Lysosomal rupture was detected after short MeHg-exposure (1 μM, 1 h) in cells maintaining plasma membrane integrity. Disruption of lysosomes was also observed after hydrogen peroxide (H2O2) exposure (100 μM, 1 h), supporting the hypothesis that lysosomal membranes represent a possible target of agents causing oxidative stress. The lysosomal alterations induced by MeHg and H2O2 preceded a decrease of the mitochondrial potential. At later time points, both toxic agents caused the appearance of cells with apoptotic morphology, chromatin condensation, and regular DNA fragmentation. However, MeHg and H2O2 stimulated divergent pathways, with caspases being activated only by H2O2. The caspase inhibitor z-VAD-fmk did not prevent DNA fragmentation induced by H2O2, suggesting that the formation of high-molecular-weight DNA fragments was caspase independent with both MeHg and H2O2. The data point to the possibility that lysosomal hydrolytic enzymes act as executor factors in D384 cell death induced by oxidative stress.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinsk bioteknologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Medical Biotechnology (hsv//eng)
Nyckelord
- Methylmercury
- Hydrogen peroxide
- Lysosomes
- Mitochondrial potential
- Caspases
- DNA fragmentation
- Free radicals
- MEDICINE
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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