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Role of Transport in Chemically-Induced Nephrotoxicity *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
No one will doubt that the administration of mercuric chloride in a sufficient dose will produce renal failure in mammalian species. Furthermore, there is little doubt that this highly predictable result is a consequence of the accumulation of mercuric ion by renal tissue. For example, the mouse accumulates as much as 60 to 80% of a given dose shortly after administration (Suzuki and Ozaki, 1984), while the rat accumulates somewhat less, 25 to 30% (Klonne and Johnson, 1983). In both species renal damage is reported.
Models of Toxicity Screening Using Cultured Cells
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Roberta L. Grant, Daniel Acosta
As these primary cultures of renal cortical epithelial cells retained differentiated functions for an extended period, they should be useful tools for the in vitro evaluation of nephrotoxic agents. To establish the validity of primary renal cell cultures as a toxicological tool, it is necessary to evaluate several compounds known to be nephrotoxic in vivo. The evaluation of known nephrotoxic agents establishes guidelines for determining toxicity. Criteria delineated by changes in organ-specific functions, organellar functions, and cell morphology can then be applied to the evaluation of potential nephrotoxins in vitro. Accordingly, three well-known nephrotoxic agents were tested: mercuric chloride, cadmium chloride, and acetaminophen. Mercuric chloride and cadmium chloride, both heavy metals, cause renal dysfunction in man. Acetaminophen, a prototype of analgesic-induced nephrotoxicity, was chosen because metabolism has been implicated in its ability to cause damage. Each of the nephrotoxins showed different patterns of toxicity.
Environmental toxicants on Leydig cell function
Published in C. Yan Cheng, Spermatogenesis, 2018
Leping Ye, Xiaoheng Li, Xiaomin Chen, Qingquan Lian, Ren-Shan Ge
Mercury is a heavy metal. Mercury pollution in industry is often in an inorganic form. However, organic mercury compounds, such as methylmercury, are concentrated in the food chain because it can be produced inside fish when they are exposed to inorganic mercury. Exposure to methylmercury (20 mg/L) via drinking water to rats for 8 weeks reduced plasma testosterone levels.243 Oral exposure to mercuric chloride at doses of 0.01, 0.05, and 0.1 μg/mL for 1–7 months caused Leydig cell death.243
Mercuric chloride poisoning: symptoms, analysis, therapies, and autoptic findings. A review of the literature
Published in Critical Reviews in Toxicology, 2019
Simone Cappelletti, Daria Piacentino, Vittorio Fineschi, Paola Frati, Stefano D’Errico, Mariarosaria Aromatario
Mercuric chloride has a relative molecular mass of 271.52 Dalton, a melting point of 277 °C, and a boiling point of 302 °C. It has a vapor pressure of 0.1 kPa at 136.2 °C and a water solubility of 28.6 g/L, which increases to 476 g/L in boiling water; its solubility in alcohol is of 263 g/L (WHO 2003). Mercuric chloride is currently used as a catalyst or reagent in several chemical reactions, and to a lesser extent as a disinfectant or pesticide (Worth et al. 1984). Potential sources of mercuric chloride intoxications are represented by mercuric chloride-containing stool preservatives (Seidel 1980), Ayurvedic medicines remedies (Indian herbo-metallic preparations) (Kew et al. 1993; Kamath et al. 2012; Kumar et al. 2015), mainly containing Rasasindura – a preparation consisting of mercuric sulfide, mixed with honey, milk, butter, or ghee. The latter, which are not subject to Food and Drug Administration (FDA) and European Medicine Agency (EMA) regulation are easily available without prescription (Young-Jin 2011).
Mercurius solubilis attenuates scopolamine-induced memory deficits and enhances the motor coordination in mice
Published in International Journal of Neuroscience, 2018
Simranjeet Kaur, Anudeep Kaur, Gurjit Singh, Rajbir Bhatti
Studies have revealed that treatment with 30X and 200X potencies of merc sol ameliorate the deleterious effects of mercuric chloride [17]. Mercuric chloride is an alarming environmental contaminant with severe health risks. Accidental and chronic exposure to mercury compounds is documented to participate in severe health hazards including minamata disease that is due to exposure of methyl mercury [35]. Post-mortem analysis of brain regions and blood of some patients with Alzheimer's disease (AD) has been shown to reveal high mercury concentrations [36]. Studies have shown that immunosuppression is also caused by exposure to mercury [8]. Mercurius treatment has been reported to improve lack of cognition and concentration and behavioural impairment in several case reports [37].
Protective Effect of Leaf Ethanolic Extract Etlingera hemisphaerica Blume Against Mercuric Chloride Toxicity in Blood of Mice
Published in Journal of Dietary Supplements, 2019
Aceng Ruyani, Rendi Zulni Eka Putri, Pauzi Jundara, Efri Gresinta, Irwandi Ansori, Agus Sundaryono
Hg poisoning is a disease caused by exposure to Hg compounds. Hg occurs in three forms (elementary, inorganic compounds, and organic compounds), which can produce toxic effects in high enough dosages. The toxic effects include damage to the lungs, brain, and kidney. Symptoms of Hg poisoning typically include disturbed sensation, sensory impairment (speech, vision, and hearing), and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, dosage, method, and duration of exposure, and then can result in several diseases, including acrodynia (pink disease; Bjørklund, 1995). Compounds of mercury tend to be much more toxic than the salts such as mercuric chloride (HgCl2). Detoxification of organomercury compounds requires special techniques (Zheng et al., 2012), which are not described in this article. HgCl2 affects primarily the gastrointestinal tract and the kidneys, can cause severe kidney damage, and can inflict neurological damage without continuous or heavy exposure. Immediate chelation therapy is the standard of care for a patient showing symptoms of severe Hg poisoning or the laboratory evidence of a large total Hg load. Chelation therapy for acute inorganic Hg poisoning can be done with succinate or meso-2,3-dimercaptosuccinate (DMSA), 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (Risher and Amler, 2005). Experimental findings in the lab have successfully demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium can help protect against the adverse effects of methylmercury (Watanabe, 2002). There is an example that chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of ethylenediaminetetraacetic acid (EDTA) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy (Baxter and Krenzelok, 2008).