Acute mercuric chloride poisoning at a potentially lethal dose ended with survival: symptoms, concentration in cerebrospinal fluid, treatment.

This study aims to present a case of acute mercuric chloride poisoning at a potentially lethal dose treated with the antidote - 2,3-dimercapto- 1-propanesulfonic acid (DMPS) and continuous renal replacement therapy (CRRT) combined with CytoSorb. A 21-year-old woman was admitted to a hospital with abdominal pain, vomiting, and suspected gastrointestinal bleeding after taking 5000 mg of mercuric chloride for suicidal purposes. Due to the patient deteriorating general condition and multiple organ damage, on the third day she was transported to the Clinic of Anaesthesiology and Intensive Care (CAaIC), Lódz, Poland. Laboratory tests confirmed features of acute kidney injury and high mercury levels in the blood (1051 µg/l) and urine (22 960 µg/l) - DMPS therapy and CRRT combined with CytoSorb were instituted. Due to nervous system complaints (headache, dizziness), a lumbosacral puncture was performed - the mercury concentration in the cerebrospinal fluid (CSF) was 5.45 µg/l. During a colonoscopy, significant diagnostic abnormalities revealed features of colonic mucosal necrosis. The treatment resulted in a decrease in subjective complaints, decreased mercury levels in biological material, and improved parenchymal organ function. On the 15th day of therapy, the patient was transferred to the primary care center for further treatment. The case confirms the possibility of improvement of patient condition following ingestion of a potentially lethal dose (5 g) as a result of the initiation of appropriate therapy even on the third day. The presence of mercury in CSF confirms that inorganic mercury compounds (mercuric chloride) can pass through the blood-brain barrier after oral ingestion. Int J Occup Med Environ Health. 2023;36(5):685-92.

Acute intranasal intoxication with mercuric chloride taken accidently instead of cocaine - A case report.

CONTEXT: Mercuric chloride (mercury (II) chloride) belongs to inorganic mercury compounds characterized by good water solubility and associated high toxicity. The paper describes an unusual case of intranasal intoxication with corrosive sublimate confused with cocaine by a young male. CASE REPORT: Intranasal administration of corrosive sublimate caused severe local symptoms of chemical burn within the nasal cavity. From the 2nd day the patient developed symptoms of renal dysfunction with transient polyuria and serum retention of nitrogen metabolites. The patient was undergoing chelation therapy with DMPS, N-acetylcysteine and d-penicyllamine. Four procedures of haemodialysis were performed with simultaneous DMPS and N-acetylcysteine treatment. The urine mercury level on the first day of hospitalization was 1989 µg/L, and after 26 days of treatment returned to the physiological level. During treatment renal function was normalized, the patient was discharged in general good condition. DISCUSSION: Mercuric chloride is readily absorbed from the nasal cavity. Its administration may cause intoxication manifested by both chemical burn at the exposure site and systemic symptoms, particularly renal impairment. Even in case of renal dysfunction the use of DMPS seems safe, if haemodialysis is performed at the same time. Simultaneous haemodialysis and chelation therapy may accelerate elimination of mercury from the organism.

The role of endoplasmic reticulum stress in renal damage caused by acute mercury chloride poisoning.

Acute mercury chloride (HgCl2) poisoning may lead to kidney injury, but the underlying mechanism remains largely unknown. Endoplasmic reticulum (ER) stress plays a role in some heavy metal poisoning. Whether it mediates kidney injury in acute HgCl2 poisoning remains unknown. In this study, we examined the kidney injury and the corresponding ER stress in the mouse model of different doses of acute HgCl2 poisoning. To further confirm the role of ER stress, we tested the effects of its chemical chaperone [4-phenylbutyric acid (4-PBA)]. The results revealed that acute HgCl2 poisoning caused more severe kidney injury with dose on and activated ER stress, as indicated by increased expression of GRP78 and CHOP. Inhibition of ER stress restored the functional and morphological changes of kidneys, and partly attenuated renal tubular epithelial cell apoptosis. In summary, ER stress contributes to the acute kidney injury following HgCl2 poisoning, and inhibition of ER stress may alleviate the kidney injury via reducing apoptosis.

Glutathione Peroxidase-Activatable Two-Photon Ratiometric Fluorescent Probe for Redox Mechanism Research in Aging and Mercury Exposure Mice Models.

Solid evidence confirms that glutathione peroxidase (GPx) is a kind of vital protease in the first-line antioxidant defense system and participates in regulation of redox homeostasis as well as the pentose phosphate pathway. However, the current methods cannot achieve real-time and in situ visualization studies of GPx. In addition, GPx is highly reactive and susceptible to external interference, and there is rare research for exploring the roles of GPx under environmental factor exposure. Herein, we report a novel two-photon ratiometric fluorescent probe (TP-SS) for GPx detection for the first time. Using TP-SS, we explore the reversible catalytic cycle and the antioxidant mechanisms of GPx/GSH redox pool in aging and mercury exposure models. We detect the concentration fluctuation of GPx in aging and mercury exposure mice models. Also, we perform GPx detection in deep brain tissue and the imaging depth up to 100 µm. We believe that the novel two-photon ratiometric fluorescent probe TP-SS can facilitate the development of GPx-targeting tools and offer great advances in exploring the physiological/pathological functions of GPx.

Mercuric chloride poisoning: symptoms, analysis, therapies, and autoptic findings. A review of the literature.

Among mercury-related intoxications, the re-emerging of mercuric chloride poisoning has been recently described in literature. Only sparse data, reporting the clinical symptoms, the anatomo-pathological findings, the analytical procedures or the treatment have been published and no exhaustive analysis of all these factors exists in literature. The classic symptoms associated with toxicity of mercuric chloride is a combination of renal, gastrointestinal (GI) and central nervous system (CNS) damages, eventually leading to death. Fatalities related to exposure to mercuric chloride have been reported since the nineteenth century. To date, there have been 45 published cases in the medical literature in which the intoxication or the death is attributed to mercuric chloride. In this review, we will describe the modern medical treatments, with particular attenztion to the developments of the lasts two decades, in order to provide an exhaustive description of the clinical symptoms, the post-mortem findings, and the analytical procedures to act out when mercuric chloride intoxication occurs. The analysis of the data obtained permitted us to accurately describe all the organs and apparatus involved in mercuric chloride intoxication. The target organs were the kidneys, the GI tract and the CNS. A description of the analytical procedures for the determination of mercuric chloride in biological materials, to carry out in vivo and in post-mortem samples has also been described.

Copper attenuates early and late biochemical alterations induced by inorganic mercury in young rats.

Mercury (Hg), a divalent metal, produces adverse effects predominantly in the renal and central nervous systems. The aim of this study was to determine the effectiveness of copper (Cu) in prevention of mercuric mercury (Hg2+)-mediated toxic effects as well as the role metallothioneins (MT) play in this protective mechanism in young rats. Wistar rats were treated subcutaneously with saline (Sal) or CuCl2.2H2O (Cu 2.6 mg/kg/day) from 3 to 7 days old and with saline or HgCl2 (Hg 3.7 mg/kg/day) from 8 to 12 days old. The experimental groups were (1) Sal-Sal, (2) Cu-Sal, (3) Sal-Hg, and (4) Cu-Hg. MTs and metal contents were determined at 13 and 33 days of age. Porphobilinogen synthase (PBG-synthase) activity as well as renal and hepatic parameters were measured at 33 days. At 13 day, Hg2+ exposure increased hepatic MT, Hg, zinc (Zn) and iron (Fe) levels, in kidney elevated Cu and Hg and decreased renal Fe concentrations, accompanied by elevated blood Hg levels. At 33 days, Hg2+ exposure inhibited renal PBG-synthase activity, increased serum urea levels and lowered Fe and Mg levels. Copper partially prevented the rise in blood Hg and liver Fe noted at 13 days; and completely blocked urea rise and diminished renal PBG-synthase activity inhibition at 33 days. In 13-day-old rats, Cu exposure redistributed the Hg in the body, decreasing hepatic and blood levels while increasing renal levels, accompanied by elevated renal and hepatic MT levels in Hg2+-exposed animals. These results suggest that hepatic MT might bind to hepatic and blood Hg for transport to the kidney in order to be excreted. ABBREVIATIONS: MT: metallothioneins; PBG-synthase: porphobilinogen synthase.

Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats.

The study was aimed to estimate whether pre-treatment with sodium selenite or taurine would reverse kidney damage induced by intraperitoneal injection of mercuric chloride in rats. Animals were divided into six groups: (1) control group; (2) sodium selenite group; (3) taurine group; (4) HgCl2 group; (5) sodium selenite pretreated group; (6) taurine pretreated group. The results demonstrated that HgCl2 causes significant enhancement in serum malondialdehyde (MDA), creatinine, N-acetyl-beta-d-glucosaminidase (NAG), cystatin C, nephrin and interleukin 6 (IL-6) levels accompanied with significant reduction in serum nitric oxide (NO) level. Pretreatment with sodium selenite or taurine produces significant depletion in MDA, NAG, cystatin C, nephrin and IL-6 levels in concomitant with significant elevation in serum NO level as compared to HgCl2 group. HgCl2 induced pathological alterations in the kidney. The ultrastructural investigation of renal cortex of HgCl2-administered group revealed that the glomerular basement membrane is uniform, the fenestrations of endothelial cells are swollen, and the secondary foot processes appear also swollen even fused at some points. The proximal convoluted tubules showed apical short and few microvilli, while, some tubular cells showed relatively normal microvilli. In contrast, sodium selenite or taurine pretreatment could significantly reduce the pathological alterations in the kidney caused by HgCl2 intoxication. The current results suggested that selenium and taurine possess nephroprotective efficacy due to their antioxidative capacity and anti-inflammatory activity.

Accidental inorganic mercury chloride poisoning in a 2-year old child.

Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life threatening features and acute renal failure. A 2-year old well thriving child presented with alleged history of accidental ingestion of inorganic mercury chloride. He presented with evidence of corrosive trauma to the gastrointestinal tract mucosa, but with normal renal function at admission, which was managed with BAL and other supportive treatment. But he developed non-oliguric renal failure after admission, which also improved gradually. On follow-up, two months later, the patient's renal function was normal; indicating that renal failure caused by acute inorganic mercury poisoning produced no permanent renal damage. We have hereby presented a case of mercury intoxication in a 2-year old child, with an excellent clinical improvement and normalization of laboratory results.

Protective effect of mycophenolate mofetil on mercuric chloride-induced nephrotoxicity in rats.

In the present study the effect of mycophenolate mofetil (MMF), an immunosuppressant, on mercuric chloride (HgCl(2))-induced nephrotoxicity in male Wistar rats was investigated. Animals (200-250 g) were divided into five groups and were subjected to a 6-day treatment schedule. The first (control) group received only vehicle without any active drug. The second to fifth groups were administered HgCl(2) challenge (single dose of 5 mg/kg, s.c.) on the fourth day. Additionally, the second group received distilled water (DW) on all 6 days and the third group was administered DW the initial 3 days and MMF (10 mg/kg b.i.d. by oral gavage) on days 4-6. The fourth group was given DW the initial 2 days and MMF on days 3-6 and the fifth group received MMF all 6 days. All animals were euthanized on the sixth day. It was found that HgCl(2) administration caused significant nephrotoxicity, as indicated by a rise in serum creatinine, blood urea and soluble intercellular adhesion molecule 1 (sICAM-1) concentrations, histopathological injury and increased oxidative stress (altered malondialdehyde and glutathione levels) as compared to the control group. Administration of MMF significantly ameliorated HgCl(2)-induced nephrotoxicity. The results suggest the potential of MMF in preventing the acute nephrotoxicity of HgCl(2).

Acute mercury intoxication and use of chelating agents.

There is a great hazard of mercury intoxication in the third world for artisanal miners using mercury as amalgam for extracting and refining gold. In developing countries, there is the possibility of risk regarding exposure to Hg from amalgam tooth fillings, ethyl-Hg (thimerosal) added as antiseptic to vaccines and methyl-Hg in fish. In one case, a 41-year-old man attempted suicide by ingesting 100 mg of HgCl2. After 8 hours, he developed hematemesis and entered the intensive care unit; his urinary Hg was 10.1 mg/l. Treatment with 2,3-dimercaptopropanol (BAL) was started by intramuscular route after 16 hours at the dosage of 5 mg/kg body weight every 4 hours on days 2-3 and 3 mg/kg every 6 hours on days 4-5 and then every 12 hours on days 6-14 without adverse side effects. Acute Hg intoxication can be managed with BAL as first choice chelator, whereas the less toxic 2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercaptopropane-1-sulfonic acid (DMPS) should be reserved for cases of less severe inorganic Hg or methyl-Hg acute intoxication. Such agents, recommended only for the treatment of acute Hg poisoning, should not be used for patients suffering from neurological diseases in which environmental Hg exposure is hypothesised.

ZnCl2 exposure protects against behavioral and acetylcholinesterase changes induced by HgCl2.

This study examined the effects of inorganic mercury exposure on behavioral and biochemical parameters and investigated the possible preventive effects of zinc on the alterations induced by mercury. Pups were exposed from 3rd to 7th postnatal day to ZnCl2 (27 mg/kg/day, s.c.) and subsequently to HgCl2 (5 doses of 5 mg/kg/day, s.c.). Each litter contained two rats for each treatment. The rats were submitted to behavioral task and litters were killed at 13 or 33 days old for acetylcholinesterase activity assays and for the determination of metal levels. Based on the results obtained from 13-day-old rats, they were divided in two groups of litters that were defined at the end of the experimental period (33 days) as less sensitive rats to mercury and more sensitive rats to mercury in accordance with the recovery of body weight until day 33. The mercury exposure caused accumulation of this metal in cerebrum and cerebellum in all mercury treated rats, and inhibited the cerebellum acetylcholinesterase activity from 13-day-old rats. Besides, the mercury-animals of the most sensitive litters to mercury presented impairment in motor function and muscular strength verified in the beaker test, as well as a reduction of the locomotor and exploratory activities in the open field task. Zinc partially prevented all the alterations induced by mercury exposure and reduced the mercury level accumulated in cerebrum and cerebellum. This study confirms the preventive effect of zinc on behavioral alterations induced by mercury in young rats and demonstrates that the mercury behavioral effects are present even for a long time after the end of the exposure.

Post-mortem CT findings following intentional ingestion of mercuric chloride.

Mercury is known to be associated with both acute and chronic poisoning. A 36-year-old man intentionally ingested mercuric chloride (HgCl(2)) and died within 24h. Post-mortem CT images showed oral, esophageal and gastric wall hyperdense "staining". On toxicological analysis, the blood concentration of mercury was measured at 25.5mg/L; a figure far higher than reported lethal levels. Autopsy was not performed in order to prevent potential inhalation of mercury vapor by pathology staff.

Mercury fatal intoxication: two case reports.

We report two cases of fatal intoxications with mercury, one intentional and the other allegedly resulting from a drug formulation mistake. Both cases occurred in the year of 2004. The first case refers to a man who ingested a great portion of a mercuric chloride solution. He attended a hospital emergency, submitted to treatment, but died after 49 days. In the second case, a woman applied on the chest skin an ointment containing a great quantity of mercury bromide. After 7 days of treatment in the hospital, she died. In both cases, samples of tissues and organs were collected at autopsy for mercury analysis. Because methylation of mercury in humans after exposure to metallic or inorganic mercury is almost unknown, both total mercury and methylmercury were quantified in the post-mortem samples. The quantifications were carried out by Cold Vapour Generation Atomic Absorption Spectrometry for total mercury and by HPLC-UV for methylmercury. The total mercury contents found in the post-mortem fluid and tissue samples were consentaneous with mercury poisoning. For the first case, the concentrations found, expressed in microg/g wet weight, were in the liver 49.9, lung 3.27 and brain 0.33, and for blood 11.7 microg/mL. For the second case, the concentrations expressed in microg/g wet weight were in the liver 46.6, lung 14.6, brain 0.21, kidney 77.7, stomach 7.12, spleen 6.4 and heart 2.34, and for blood and urine 2.95 and 1.40 microg/mL, respectively. Only in the first case was methylmercury found and quantified in liver (1.70 microg/g wet weight) and in blood (0.15 microg/mL) samples.

Comparative evaluation of the protective effect of selenium and garlic against liver and kidney damage induced by mercury chloride in the rats.

The present study was designed to compare the protective effect of selenium and garlic against liver and kidney damage induced by (ip) injection of 0.5 mg/kg mercury chloride (HgCl(2)) in rats. Thirty-six Sprague-Dawley rats were used in the present experiment and divided into six groups: one group was orally given (1 ml) saline and served as a control group; two groups of rats were given either selenium (0.1 mg/kg) or garlic (63 mg/kg) alone, once daily an oral dose for 30 successive days; other two groups of rats were given either selenium or garlic alone, once daily a dose for 15 successive days prior to HgCl(2) injection and on the next 15 successive days simultaneously with HgCl(2) injection; and the last group of rats was injected ip with HgCl(2) for 15 days and at the end of the experiment (which lasted 30 days), blood samples for the biochemical analysis were obtained from all rats after being lightly anesthetized with ether, and specimens of kidney and liver were removed and prepared for histochemical study. Computer image analysis was applied to liver and kidney tissues to evaluate the DNA density and DNA ploidy pattern in different groups. The results revealed that the rats injected with HgCl(2) showed a significant increase in levels of blood urea nitrogen (BUN), serum creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST) by 29.3%, 62.5%, 29.46% and 30.61%, respectively, while alkaline phosphatase (ALP) showed a significant decrease by 22.6% as compared with saline control group. Rats that were given selenium in combination with the HgCl(2) injection showed a significant decrease in BUN, Serum creatinine, ALT and AST levels, while ALP was significantly increased as compared with HgCl(2) group. Also rats that were given garlic in combination with HgCl(2) injection showed a significant decrease in BUN, Serum creatinine, ALT and AST levels, although serum ALP level showed an increase as compared to HgCl(2) group. Rats that had been orally administered selenium or garlic alone did not show any significant changes in the serum level of BUN, Serum creatinine, ALT and AST but there was a significant decrease in ALP level as compared with saline control group. The cytometric results revealed that injection of HgCl(2) induced an increase in the DNA density in kidney tissues with an increase in aneuploid cells and decrease in diploid cells. However, DNA density decreased in liver tissues with mild decrease in diploid cells and little percentage of aneuploid cells. We can conclude that oral administration of either selenium or garlic produces a significant protection against liver and kidney damage induced by the HgCl(2) injection, but garlic appears to be more protective.

Baboon syndrome induced by mercury - first case report in China.

A case of mercury-induced baboon syndrome was reported. A 31-year-old woman presented with itching papules and vesicles in the right axilla, which extended to the left axilla, arms, fossa poplitea, buttocks, and groin. A mercury thermometer was broken 2 days before exanthema. Patch testing to ammoniated mercury, mercury, mercuric chloride, and mercurochrome were positive. Blood and urine mercury level was marginally normal, yet showed a descending trend over time.

Successful treatment of potentially fatal heavy metal poisonings.

Pure inorganic heavy metal ingestions for suicidal intent are a rare occurrence. Most case reports on this subject focus on the serious neurological, hepatic, or renal side effects. We describe two cases of significant heavy metal poisonings (arsenic trioxide and mercuric chloride) that were successfully managed with aggressive decontamination and combined chelation therapy. Both chemicals were obtained in pure powder form through the Internet.

Recovery of phosphatase and transaminase activity of mercury intoxicated Mus musculus (Linn.) liver tissue by Tribulus terrestris (Linn.) (Zygophyllaceae) extract.

The efficacy of the methanolic fraction (MF) of Tribulus terrestris fruit extract on mercury intoxicated mice, Mus musculus has been studied. At a median-lethal dose of mercuric chloride (12.9 mg/kg body wt.) administration an enhanced level of glutamate oxaloacete transaminase (GOT), glutamate pyruvate transminase (GPT) and simultaneously decreased level of acid phosphatase (ACP) and alkaline phosphatase (ALT) activities were noticed in the liver. Due to the mercury toxicity the liver cells are damaged to cause the alterations in their enzymes. During the recovery period, all the enzymological parameters are restored to reach near normal level. The result suggested that the oral administration of MF of T. terrestris fruit extract has (6 mg/kg body wt.) provided protection against the mercuric chloride induced hepatic damage in the mice, M. musculus.