IMercuric chloride (HgCl2) is a very poisonous salt and was once used to disinfect wounds. Mercurous chloride (Hg2Cl2), also called calomel, is an antiseptic used to kill bacteria.
Mercury is poisonous and can enter the body through the respiratory tract, the digestive tract or directly through the skin. It accumulates in the body, eventually causing severe illness or death.
Mercurous chloride is toxic, although due to its low solubility in water it is generally less dangerous than its mercuric chloride counterpart.
Identifying and removing the source of the mercury is crucial. Decontamination requires removal of clothes, washing skin with soap and water, and flushing the eyes with saline solution as needed. Inorganic ingestion such as mercuric chloride should be approached as the ingestion of any other serious caustic. Immediate chelation therapy is the standard of care for a patient showing symptoms of severe mercury poisoning or the laboratory evidence of a large total mercury load.
Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side effects, and has been found to be superior to BAL, DPCN, and DMPS. Alpha-lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and N-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain. Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.
Even if the patient has no symptoms or documented history of mercury exposure, a minority of physicians (predominantly those in alternative medicine) use chelation to "rid" the body of mercury, which they believe to cause neurological and other disorders. A common practice is to challenge the patient's body with a chelation agent, collect urine samples, and then use laboratory reports to diagnose the patient with toxic levels of mercury; often no pre-chelation urine sample is collected for comparison. The patient is then advised to undergo further chelation. No scientific data supports the claim that the mercury in vaccines causes autism or its symptoms, and there is no scientific support for chelation therapy as a treatment for autism.
Chelation therapy can be hazardous. In August 2005, an incorrect form of EDTA used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.
Many of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. However, heavy or prolonged exposure can do irreversible damage, particularly in fetuses, infants, and young children. Young's syndrome is believed to be a long term consequence of early childhood mercury poisoning.n type-II diabetes, insulin resistance, As opposed to a Deficiency of insulin, May be the Reason for elevated Bloodstream glucose levels. A tiny Quantity of clinical Examine have reported the benefits of Large doses of racemic Lipoic Acids in Enhancing insulin sensitivity. Animal Examine have Recommended Greater Advantage Amounts from R-isomer of Lipoic Acid as In comparison with its S-isomer. However, clinical Examine are Necessary to Confirm this benefit. Evidence of Lipoic Acid-induced Decrease of oxidative Worry in diabetic patients’ Must Grow to be Founded with Even more studies.
The Valuable Consequences Of theLA Remedy on Signs or symptoms of diabetic neuropathy Happen to be Discovered in No Much less than 15 clinical trials. Many short-term preliminary Examine in Human beings have stated that Lipoic Acid Management can Decrease the Chance of vascular Problems in diabetic (type I and Kind II) patients.
Several Examine In a veryging rats have reported that short-term Mixed dietary supplementation with R-alpha Lipoic Acid Plus acetyl-L-carnitine Enhanced mitochondrial Power metabolism, Reduced oxidative stress, and Experienced Optimistic Consequences on Actual physical Action and short-term memory. However, long-term Examine on Human beings are Required to Confirm Comparable effects. In a Quite short-term Examine study, Lipoic Acid Continues to be Discovered to Appreciably Boost plasma Nutritional C and glutathione in HIV-infected patients. In a Quite Russian study, Lipoic Acid’s Capability To Minimize Back again Absolutely free radical Harm Brought on by radiation Coverage Continues to be observed.
Animal Examine have reported Using Lipoic Acid While in the prevention of Cellular Harm in stroke and congestive cardiac failure patients. Extensive animal Examine have Proven the Considerable protective Consequences of Lipoic Acid Towards ischemia-reperfusion injury. Animal Examine on Lipoic Acid Possess also proposed its Advantage While in the Remedy of Various neurodegenerative disorders, Such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. While The Effects Of thenimal Examine are encouraging, long-term, placebo-controlled, randomized clinical trials are Required for its Self-confident prescription.