Induction of apoptosis by mercury compounds depends on maturation and is not associated with microglial activation

Monnet‐Tschudi, Florianne

doi:10.1002/(sici)1097-4547(19980801)53:3<361::aid-jnr10>3.0.co;2-8

Cited by 35 publications

(18 citation statements)

References 31 publications

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“…Studies with EtHgCI and PhHgCI and T cells produced similar dose-dependent results. Recent studies in the brain have demonstrated accelerated spontaneous apoptosis of immature astrocytes by HgC12 added to rat brain cell cultures (152). DNA synthesis was decreased, and associated with calcium influx and tyrosine phosphorylation by 10 pM HgCl2 (153).…”

Section: Ironmentioning

confidence: 99%

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Kelleher

Pacheco

Newman

2000

Environ Health Perspect

150

117

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In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility. Key words: aluminum, beryllium, cadmium, cobalt, copper, hard metal disease, iron, mercury, metal fume fever, nickel, pneumoconiosis. The term pneumoconiosis, first introduced in the 19th century, refers to diseases and pathologic consequences from inhalation of particulate dusts. In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metalinduced parenchymal lung disorders. As presented in Table 1 (1). A major theme that emerges in reviewing recent developments in metal-related lung toxicity is the extent to which various metals are capable of inducing both antigen-specific immunologic reactions in the lung and nonspecific "innate" immune system responses characterized by inflammation frequently triggered by oxidant injury. With the recognition of these immune and inflammatory effects comes a growing awareness of the potential hazards to the lung at low levels of exposure. There is also increasing research being conducted on the interaction between metal exposure and the human genome. In the cases of beryllium and cobalt, for example, there is emerging recognition of the spec...

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Section: Ironmentioning

confidence: 99%

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Kelleher

Pacheco

Newman

2000

Environ Health Perspect

150

117

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“…In vitro studies produced the following results: Mercury interferes with polymerization of microtubules [122,123], increases secretion of both 1-40 and 1-42 forms of Aβ and promotes hyperphosphorylation of tau protein [9,[124][125][126][127], changes mitochondrial structure inducing a stress-response in astrocytes [128], and interferes with cell-maturation [129] or other aspects of cell functioning, such as DNA repair, glutathione level, or linkage and structure of microtubules [119,130,131]. Mercury disturbs the interaction between tubulin and GTP [132], and the chelator DMSA can reverse this process [133], while amalgam exposure is toxic for nerve cells in vitro [134].…”

Section: Experimental Animal and In Vitro Studiesmentioning

confidence: 99%

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Mutter¹,

Curth

Naumann³

et al. 2010

JAD

147

113

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Abstract. Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol. Two reviewers extracted relevant data independent of each other. One thousand and forty one references were scrutinized, and 106 studies fulfilled the inclusion criteria. Most studies were case control or comparative cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible.

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“…40 Exposure of cultured cerebellar granule cells to 28 mM ethanol (a physiological concentration) inhibited differentiation, migration on a laminin substratum, and resulted in death by apoptosis. 37 Methylmercury has been shown in vitro to induce apoptosis in fetal rat telencephalon, 41 developing murine cerebellar granule neurons, 42 and rat cerebellar slice cultures. 43 In cerebellar slices, mercury produced a dose-dependent inhibition of migration of external granule cells and was accompanied by apoptosis of the non-migrating cells.…”

Section: Other Regionsmentioning

confidence: 99%

Qualitative and quantitative estimates of apoptosis from birth to senescence in the rat brain

White

Barone

2001

Cell Death Differ

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Apoptosis is crucial for proper development of the CNS, wherein a significant percentage of all central neurons produced during early ontogeny die by apoptosis. To characterize the pattern of developmental programmed cell death, we assayed rat brainstem, neocortex, hippocampus, and cerebellum from birth through senescence. Quantitatively, using an ELISA for oligonucleosomal DNA fragments, we demonstrated that PND1 brainstem, neocortex, and hippocampus have the highest levels of fragmented DNA compared to older ages. Cerebellum displayed a large peak at PND10 and a smaller peak at PND21. Low levels were observed throughout adulthood and into senescence, which was corroborated qualitatively by agarose gel and TUNEL data. These data provide a temporal and regional baseline for further studies of the effects of perturbations of cell death during neural development. Quantitative and qualitative changes in these regional profiles of apoptosis due to environmental insults during early ontogeny may alter neuron number and function later in life. Cell Death and Differentiation (2001) 8, 345 ± 356.

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Induction of apoptosis by mercury compounds depends on maturation and is not associated with microglial activation

Cited by 35 publications

References 31 publications

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Inorganic dust pneumonias: the metal-related parenchymal disorders.

Does Inorganic Mercury Play a Role in Alzheimer's Disease? A Systematic Review and an Integrated Molecular Mechanism

Qualitative and quantitative estimates of apoptosis from birth to senescence in the rat brain

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