PeerJ · 2016 · 50 citations · 51 references
Veterinary MedicineDevelopmental BiologyToxicologyDevelopmental ToxicologyEmbryogenesisHeavy Metal ToxicologyDevelopmental NeurotoxicityDevelopmental ToxicityHeavy Metal Reproductive ToxicityMercury ToxicologyMetal ToxicityNeurotoxicity In Aquatic OrganismsEmbryonic NeurotoxicityHeart Tube FormationHeavy Metal Developmental ToxicityInorganic Mercury ToxicityPericardial EdemaPigmentationReproductive Development ToxicityToxicity Of Mercury Exposure
This study examined developmental toxicity of different mercury compounds, including some used in traditional medicines. Medaka (Oryzias latipes) embryos were exposed to 0.001-10 µM concentrations of MeHg, HgCl2, α-HgS (Zhu Sha), and β-HgS (Zuotai) from stage 10 (6-7 hpf) to 10 days post fertilization (dpf). Of the forms of mercury in this study, the organic form (MeHg) proved the most toxic followed by inorganic mercury (HgCl2), both producing embryo developmental toxicity. Altered phenotypes included pericardial edema with elongated or tube heart, reduction of eye pigmentation, and failure of swim bladder inflation. Both α-HgS and β-HgS were less toxic than MeHg and HgCl2. Total RNA was extracted from survivors three days after exposure to MeHg (0.1 µM), HgCl2 (1 µM), α-HgS (10 µM), or β-HgS (10 µM) to examine toxicity-related gene expression. MeHg and HgCl2 markedly induced metallothionein (MT) and heme oxygenase-1 (Ho-1), while α-HgS and β-HgS failed to induce either gene. Chemical forms of mercury compounds proved to be a major determinant in their developmental toxicity.
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Mutation of the mouse klotho gene leads to a syndrome resembling ageing.
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The pharmacological basis of therapeutics
Isaac Starr · American Heart Journal · 1941 · 1.9K citations