Review article: acute inorganic mercury vapor inhalation poisoning.

Mercury contamination is a serious environmental problem worldwide. Two primary sources of contamination are dumping of large quantities of inorganic mercury and exposure in the mining industry. Although the actual fatal level of mercury vapor is not known, exposure to more than 1-2 mg/m3 of elemental mercury vapor (Hg0) for a few hours causes acute chemical bronchiolitis and pneumonitis. Two hours after exposure, lung injury appears as hyaline membrane formation, and finally, extensive pulmonary fibrosis occurs. Clinical findings correlate with the duration of exposure, the concentration of mercury, and the survival time after exposure. There is no correlation between pathological findings and the concentration of mercury in the tissues. Necrosis of proximal convoluted tubules may be attributed to the disruption of the enzyme systems of Hg2+-sulfhydryl compounds. Metallothionein protein (MT), induced by the accumulation of Hg2+ in the kidneys, may play an important role in detoxication after it forms a non-toxic Hg2+-MT compound. Despite the deposition of mercury in the brain, compared with organic mercury, inorganic mercury did not seem to damage the neurons. Drugs such as chelating agents and corticosteroids appear to effectively decrease the inflammation and delay pulmonary fibrosis.

A rare fatal case of silicone resin precursor (SH792) poisoning.

A 39-year-old man committed suicide by ingesting a large quantity of SH792. SH792 is a silicone resin precursor used as a hardener for waterproof paints. It is polymerized in water; this process is then followed by the formation of silicone resin and the release of N,N-diethylhydroxylamine. In this decedent, analysis by infrared spectroscopy showed that polymerized silicone resin was present in the stomach contents. The amount of silica in his tissues was within levels seen in control subjects. N,N-diethylhydroxylamine was detected in the urine (0.7 microliters/ml) but not in the stomach contents. The data suggest that SH792 was polymerized in the stomach and the released N,N-diethylhydroxylamine (DEHA) was absorbed into the body. The mechanism of SH792 poisoning is also discussed.

Alpha-2-HS-glycoprotein phenotype frequencies in Cook Islanders.

The polymorphism of the alpha 2-HS-glycoprotein (A2HS) was analysed in Rarotonga and Mangaia, the Cook Islands. The A2HS*2 frequency was found to be the highest value among all populations studied up to now. There was a significant difference in A2HS*2 gene frequencies between the two populations, Rarotonga (0.62) and Mangaia (0.76).

The use of calcium hydroxyapatite ceramic in bone tumour surgery.

We report 60 benign bone tumours treated by resection and curettage followed by the implantation of calcium hydroxyapatite ceramic (CHA). After follow-up of six to 60 months (average 36), no patient had local recurrence of the tumour or any adverse effects from the implants. In almost all cases radiography showed that the CHA was well-incorporated into the host bone, with new bone formation in and around the CHA. Corrective remodelling of deformed bone and normal fracture healing suggested that there was normal bone turnover in the presence of the CHA. Histology of biopsies from seven patients showed bone ingrowth into the pore structure of CHA in the central zone of some defects by one year after implantation. CHA appears to be a useful substitute for bone graft in the treatment of some benign tumours.

Changes of leukotrienes in rabbits subjected to tourniquet shock.

Rabbits were used as a traumatic shock model, and the right femoral root was fastened tightly with a tourniquet for human children for 24 hours. The amounts of LTB4, LTD4 and LTE4 in the blood and muscle were measured just before unfastening and 3, 6 and 12 hours after unfastening. After unfastening, the rabbits showed a gradual decline of blood pressure, and one died 7 hours after unfastening. LTB4 levels in the blood and muscle were within the levels of the control rabbits throughout the experimental period. On the contrary, LTD4 levels in the blood increased just before and 6 and 12 hours after unfastening. LTD4 levels in the muscle also increased at the fastened site just before and 3 and 6 hours after unfastening. LTE4 levels in the blood increased 3 hours, and those in the muscle 3 and 6 hours after unfastening. These results suggest that peptide leukotrienes may contribute to the pathogenesis of traumatic shock.

Distribution of orosomucoid (ORM1) phenotypes in Cook Islanders: analysis by six-band patterns.

The polymorphism of the orosomucoid (ORM) system was analysed in 318 Cook Islanders. Modified isoelectric focusing revealed six-band patterns in thin-layer polyacrylamide gel followed by immunofixation. The first ORM locus showed four-band patterns with variations, while the second locus revealed two-band patterns without variation. ORM1*1 and ORM1*2 gene frequencies were 0.7893 and 0.2107 respectively. ORM1*3 allele was not detected.

Copper-binding protein in acute copper poisoning.

This paper presents a suicide case of copper sulfate ingestion. Post-mortem autopsy revealed mucous membrane necrosis of the esophagus and the stomach. Histological examination revealed centrilobular necrosis in the liver and renal insufficiency. The quantitative determination of copper, zinc and cadmium in various tissues showed that the copper concentrations in blood, liver, kidney and lung were 3.5-24-fold higher than those of the normal level, whereas zinc and cadmium concentrations were within normal range. Chromatographical patterns on Sephadex G-75 showed that most of the accumulated copper in the liver and kidney was bound to metallothionein (MT), a low molecular weight protein with high metal binding capacity which plays a role in the detoxification of heavy metals, while no copper bound to MT was found in the lung. These results suggest that the formation of Cu-induced MT in the liver and kidney occurred at the early stage in fatal acute copper poisoning.

Lipid peroxidation in human paraquat poisoning.

The concentration of malondialdehyde (MDA) in tissues in paraquat poisoning was compared between humans and rats. Lung MDA increased in humans, but not in rats despite of development of histological change of the lung. On the other hand, liver MDA increased both in humans and in rats. These findings suggest that lipid peroxidation may not be primary mechanism of paraquat toxicity.

A comparative study on the effects of paraquat and diquat on cultured human cells.

The effects of paraquat on human embryonic somatic cells were compared with those of diquat, which is a bipyridylium compound similar to paraquat. Cell lesions, mainly fatty degeneration, were observed after staining with Sudan Black B. Both herbicides caused fatty degeneration in the cells even at a concentration of 1 ppm; paraquat also caused more vacuolar degeneration at 200 to 400 ppm, than did diquat. Paraquat caused slightly higher lactate dehydrogenase activity than did diquat. The cell mortality was examined by staining with nigrosine and calculating the number of dead and damaged cells. The cell mortality for diquat was higher than that for paraquat at all concentrations but not significantly (p less than 0.05).

Identification of type A and type C virus particles in BF murine osteosarcoma.

Two types of virus particles, intracisternal type A and extracellular type C with budding, were detected in the same cells of BF osteosarcoma, its cultured cell lines, and their BFO tumors in CBA mice. The type C particles were approximately 100 microns in diameter. The buoyant density of the virions was 1.16g/ml in sucrose and 1.07 g/ml in Ficoll. A 72S RNA was demonstrated by gel electrophoresis, but no DNA was detected. Reverse transcriptase activity was also demonstrated in detergent-treated virions. Thus, the particles seem to be RNA virus. Cellular transformation and focus formation were observed after rat and mouse embryo cell monolayers were infected with the virus. The same kind of osteosarcoma was produced by inoculation of cloned transformed cells (BFOSV) of CBA embryo cells into CBA mice. Thus, the virus seems to be an oncornavirus.

Tissue distribution of paraquat and diquat after oral administration in rats.

The differential distribution of paraquat and diquat in liver, kidney, lung, brain and heart has been studied after oral administration of the LD50 or LD50/2 to rats. Paraquat concentrations were highest in all organs at 24 hours; at this time concentrations in kidney and lung were 2 to 3 times higher than at 2 hours. In contrast, with the exception of kidney, tissue diquat concentrations were highest at 2 hours. There was severe lung damage at 24 hours after paraquat; diquat aid not produce severe lung lesions, but caused intestinal distention and diarrhea. These findings suggest that the difference in the toxicity of paraquat and diquat is related to their difference in tissue distribution and excretion.

The effects of paraquat on cultured human embryonic cells.

The effects of paraquat on human embryonic somatic cells were studied. Monolayer cultured cells, from several different organs, were exposed to various concentrations of paraquat. Then, the cells were stained with nigrosine and Sudan IV to demonstrate dead or damaged cells and fatty granules, respectively. The lowest paraquat concentration that caused morphological changes varied from 1 to 10 ppm, and the lowest concentration that caused fatty degeneration varied from 1 to 5 ppm. In both types of staining, the lowest degenerative concentration was lower as the culture generation was younger, and the degree of degeneration did not differ with the cell origin. The protein content per cell in paraquat-treated cells was not significantly decreased in comparison with control cells.