OBJECTIVETo investigate the changes of mercury (Hg) levels in cerebrospinal fluid (CSF) in patients with chronic mercury poisoning and elucidate the neurotoxic mechanism of mercury.

METHODSNine patients with chronic mercury poisoning (poisoning group) as well as eight patients without exposure to mercury were included in this study. Mercury concentrations of 24 hour urine (U-Hg) and CSF (CSF-Hg) were measured with cold-vapor atomic absorption spectrometry-alkali stannous chloride method. The concentration of blood (B-Hg) at the same day was measured with cold-vapor atomic absorption spectrometry-acidic stannous chloride method. In five patients of poisoning group, these concentrations before chelation therapy were compared with those after chelation therapy.

RESULTSThe levels of B-Hg, U-Hg, and CSF-Hg in poisoning group (250.00 +/- 48.54, 160.07 +/- 91.15, 20.22 +/- 10.21 nmol/L, respectively) were significantly higher than those in control group (81.04 +/- 63.01, 24.73 +/- 9.96 nmol/L, undetectable, respectively; P < 0.01). In nine patients of poisoning group, CSF-Hg concentrations were correlated with B-Hg (r = 0.675, P < 0.05), but not U-Hg. After chelation therapy with dimercaptopropane sulfonate in five patients of poisoning group, the levels of B-Hg, U-Hg, and CSF-Hg were decreased significantly (P < 0.05). The reduction of CSF-Hg was not related with B-Hg and U-Hg.

CONCLUSIONCSF-Hg concentration in chronic mercury poisoning patient is increased with the rise of B-Hg, but not U-Hg. When the levels of B-Hg and U-Hg drop to normal, the CSF-Hg level is still high enough to be detected. It indicates that mercury is combined with protein after entering brain and this complex is difficult to cross through blood-cerebral barrier. The complex may cause neuromuscular disorder and fremitus in chronic mercury poisoning.

Adult ; Antidotes ; therapeutic use ; Chronic Disease ; Female ; Humans ; Male ; Mercury ; cerebrospinal fluid ; Mercury Poisoning ; cerebrospinal fluid ; drug therapy ; Middle Aged ; Occupational Exposure ; Spectrophotometry, Atomic ; Unithiol ; therapeutic use

This article made a brief analysis of clinical adverse effects of cinnabar. Except for allergic reaction, almost all the adverse events of cinnabar were caused by unreasonable application. The majority of the poisoning cases were associated with excessive and/or long-term dosage, and improper preparation methods, such as decocting, heating or fumigating. Children showed to be prone to poisoning. The poisoning caused by unreasonable use of cinnabar should be considered to be drug alert, but not advert effect. And the toxicity of cinnabar could be avoided by normalizing the preparation method, controlling the dosage and duration.
Chemical and Drug Induced Liver Injury ; etiology ; Coma ; chemically induced ; Drug Compounding ; adverse effects ; Drug Incompatibility ; Drug Overdose ; Gastrointestinal Diseases ; chemically induced ; Humans ; Hypersensitivity ; etiology ; Mercury Compounds ; adverse effects ; poisoning ; Mercury Poisoning ; prevention & control ; therapy

Objective: To explore the expulsion effect of sodium dimercaptopropanesulfonate (DMPS) on mercury in different organs of mercury poisoning and the therapeutic effect of glutathione (GSH) combined with antioxidant therapy on mercury poisoning. Methods: In February 2019, 50 SPF male SD rats were randomly divided into 5 groups, 10 rats in each group: A (saline negative control group) , B (HgCL2 positive control group) , treatment group (C: intramuscular injection of DMPS 15 mg/kg treatment, D: intramuscular injection of DMPS30 mg/kg treatment, E: intramuscular injection of DMPS 15 mg/kg and intraperitoneal injection of GSH200 mg/kg treatment) . Rats in group B, C, D and E were subcutaneously injected with mercury chloride solution (1 mg/kg) to establish a rat model of subacute mercury poisoning kidney injury. Rats in group A were subcutaneously injected with normal saline. After the establishment of the model, rats in the treatment group were injected with DMPS and GSH. Rats in group A and group B were injected with normal saline. At 21 d (treatment 7 d) and 28 d (treatment 14 d) after exposure, urine and blood samples of 5 rats in each group were collected. Blood biochemistry, urine mercury, urine microalbumin and mercury content in renal cortex, cerebral cortex and cerebellum were detected. Results: After exposure to mercury, the contents of mercury in renal cortex, cerebrum and cerebellum of rats in group B, C, D and E increased, and urine microalbumin increased. Pathology showed renal tubular injury and renal interstitial inflammation. Compared with group B, urinary mercury and renal cortex mercury in group C, D and E decreased rapidly after DMPS treatment, and there was no significant decrease in mercury levels in cerebellum and cerebral cortex of rats, accompanied by transient increase in urinary albumin after DMPS treatment (P<0.05) ; the renal interstitial inflammation in group E was improved after GSH treatment. There was a positive correlation between urinary mercury and the contents of mercury in renal cortex, cerebral cortex and cerebellum (r=0.61, 0.47, 0.48, P<0.05) . Conclusion: DMPS mercury expulsion treatment can significantly reduce the level of metal mercury in the kidney, and there is no significant change in the level of metal mercury in the cortex and cerebellum.
Animals ; Brain/drug effects* ; Glutathione ; Inflammation ; Kidney/drug effects* ; Kidney Diseases/chemically induced* ; Male ; Mercuric Chloride/therapeutic use* ; Mercury/urine* ; Mercury Poisoning/drug therapy* ; Rats ; Rats, Sprague-Dawley ; Saline Solution/therapeutic use* ; Unithiol/therapeutic use*

OBJECTIVETo study protective effect and pathogenesis of complex salvia miltiorrhiza (DanShen) on acute mercury poisoning in rabbits.

METHODSModels of acute mercury poisoning was made in rabbits. The effect of complex salvia miltiorrhiza on blood urea nitrogen (BUN), copper-protein (CP), lactate dehydrogenase (LDH), acid phosphatase (ACP) and the malondialdehyde (MDA) in plasma, superoxide dismutase (SOD) in erythrocyte and MDA, SOD in tissues homogenate were observed.

RESULTSThe administration of complex salvia miltiorrhiza after mercury injection 0.5 h and 9.5 h, decreased BUN, CP, MDA, LDH and ACP, and prevented the reduction of SOD. Compared with mercury poisoning group, the difference was statistical significant (P < 0.05, P < 0.01).

CONCLUSIONIt is suggested that acute mercury poisoning may result in renal damage but also multiple organ tissues, and complex salvia miltiorrhiza possesses protective effect, through stabilized membranes.

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Male ; Mercury Poisoning ; blood ; drug therapy ; Phenanthrolines ; pharmacology ; therapeutic use ; Rabbits ; Salvia miltiorrhiza

Acute mercury inhalation poisoning is a rare cause of acute lung injury. It is usually fatal because of progressive pulmonary failure. We experienced a patient with acute respiratory distress syndrome (ARDS) after illicit use of mercury vapor for hemorrhoid treatment; he developed acute chemical pneumonitis following exposure to mercury vapor. Prompt treatment with corticosteroids and penicillamine for acute chemical pneumonitis was instituted; radiologic pulmonary infiltrates disappeared within a week, but late phase neurologic sequelae and pulmonary interstitial fibrosis progressed.
Adrenal Cortex Hormones/administration & dosage ; Aged ; Antidotes/administration & dosage ; Disease-Free Survival ; Human ; Inhalation Exposure/adverse effects* ; Male ; Mercury Poisoning/diagnosis ; Mercury Poisoning/complications* ; Penicillamine/administration & dosage ; Respiratory Distress Syndrome, Adult/drug therapy ; Respiratory Distress Syndrome, Adult/chemically induced* ; Substances:Penicillamine ; Substances: Antidotes ; Substances: Adrenal Cortex Hormones