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A toxic and teratogenic potential ranking of sodium arsenate, sodium arsenite, and cacodylic acid by the application of the in vitro hydra assay.
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Activation of CPP 32 and internucleosomal DNA fragmentation and inactivation of poly (ADP-ribose) polymerase (PARP) during hyperthermia and sodium arsenite-induced apoptosis in early postimplantation mouse embryos.
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Altered Developmental Programming of Fetal Liver by Prenatal Arsenic Exposure Associated With Accelerated Atherogenesis in ApoE-knockout Mice.
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Antioxidant amelioration of arsenical-induced effects in vivo.
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Apoptotic signaling pathways in teratogenesis.
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Apoptotic signaling pathways.
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Arsenic as a developmental toxicant: low dose exposure in utero induces aberrant gene expression in the embryonic lung.
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Arsenic-induced heart defects in the chick embryo: the oxidative stress response.
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Arsenic-induced neural tube defects in a C57BL/6J splotch heterozygote cross.
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Caspase-3 enzyme activity as a marker for teratogen-induced apoptosis in day 9 mouse embryos and associated yolk sacs: evidence for yolk sac resistance to teratogen-induced apoptosis.
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Cell-cycling effects from in vitro exposure to sodium arsenite on developing rat midbrain cells.
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Characteristic of thymus in newborn mice after chronic exposure of their mothers to sodium arsenite.
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Effect of arsenic on cultured mouse embryos in relation to valency, gestational age and duration of exposure.
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Exposure To Arsenic Compromises Zona Escape In Hamster Embryo.
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Expression and function of the stress-inducible HSP70s during preimplantation embryogenesis.
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Female predominance among CD-1 mouse fetuses with arsenic-induced exencephaly.
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Further development and validation of the Frog Embryo Teratogenesis Assay--Xenopus (FETAX), phase III.
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Induction of a stress response and abnormal development in rat embryos exposed in vitro to sodium arsenite.
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Influence of maternal restraint stress on arsenic-induced pre- and postnatal alterations in mice.
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Inorganic arsenic compounds: are they carcinogenic, mutagenic, teratogenic?
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Meso-2,3-Dimercaptosuccinic acid (DMSA) alleviation of arsenite-induced embryofetotoxicity in mice: effectiveness with time.
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Modulation of arsenic teratogenicity by free radical scavengers.
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Periodate-oxidized adenosine, a methylation inhibitor, enhances developmental toxicity of arsenic in mice.
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Prevention by meso-2,3-dimercaptosuccinic acid (DMSA) of sodium arsenite-induced embryotoxic and teratogenic effects in mice.
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Prevention by meso-2,3-dimercaptosuccinic acid (DMSA) of sodium arsenite-induced embryotoxic effects in mice.
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Response of embryos of the sea urchin Strongylocentrotus purpuratus to aqueous petroleum waste includes the expression of a high molecular weight glycoprotein.
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Stress protein synthesis induced in chick embryos by arsenite (As), mercury (Hg), and cadmium (Cd).
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Teratogenic responses to cadmium and arsenite: relative sensitivity of C57BL/6 and SWV mice.
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Toxicogenomic analysis of aberrant gene expression in liver and liver tumors induced by transplacental exposure to inorganic arsenic in mice.
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Example Content from MEDITEXT for 7784-46-5:
Please note: this is an extract of information from a larger document. Full document and details are available by subscription.
ACUTE EXPOSURE INFORMATION
- Sodium arsenite is a trivalent, inorganic arsenical compound. It is a white or greyish powder solid.
- Sodium arsenite can cause acute and chronic arsenic poisoning following ingestion, inhalation, or dermal exposure. It is a known human carcinogen and mutagen, and has caused teratogenicity and adverse reproductive effects in experimental animals. It is advisable to treat all arsenic compounds as highly toxic.
- Acute arsenic ingestion generally produces symptoms within 30 to 60 minutes, but symptom onset may be delayed for several hours if ingested with food. A metallic or garlic taste, vomiting, abdominal pain, dysphagia, and profuse watery (rice-water-like) and sometimes bloody diarrhea may occur. Dehydration, intense thirst, and fluid-electrolyte disturbances are common. Hypovolemia from capillary leaking ("third spacing" of fluids) is a common early event.
- Systemic arsenic poisoning from occupational exposure is uncommon. Arsenic workers have developed a hoarse voice, nasal irritation and possibly perforation of the nasal septum, irritation of eyes, skin, and mucous membranes, and rarely, cirrhosis of the liver. Nausea and vomiting are infrequent complaints among arsenic workers. Painful ulceration of the wrist and scrotal skin, lips, and nostrils may develop with dust exposure.
- Initially, the primary target organs are the gastrointestinal tract, heart, brain, and kidneys. Eventually, the skin, bone marrow, and peripheral nervous system may be significantly damaged. Peripheral neuropathy appears similar regardless of the route of exposure.
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