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Biomedical subjects

T W Clarkson

Publications and source records attributed to T W Clarkson.

At least 109 records · Page 6Linked to original sources
PubMed1980

The effect of ethanol on the fate of mercury vapor inhaled by man.

Three human subjects ingested 1065 ml of beer equivalent to 65 ml of ethanol 30 min before exposure (12-20 min) to mercury vapor. An additional two subjects were exposed to mercury vapor without ethanol pretreatment. The results show that alcohol brings about: 1) reduced mercury retention, 2) an increase in the rapid phase of vapor loss by expiration, 3) an increased mercury storage in the liver, 4) a marked reduction in mercury uptake by the red blood cells and 5) the abolition of vapor exposure experiments were performed by using control and ethanol-pretreated mice and rats. Sacrifice occurred at 1 hr and 3 days. The results support and extend the human data.

Animals↗
PubMed1979

The effects of bromosulphophthalein, indocyanine green and bilirubin on the biliary excretion of methylmercury.

The effects of three ligands for ligandin on the biliary excretion of methylmercury were investigated in male rats injected intravenously with 1.0 mg/kg Hg as Me203 HgCl. Bromosulphophthalein and indocyanine green inhibited the biliary excretion of methylmercury, while bilirubin had no such effect. None of the compounds tested which inhibited the biliary excretion of methylmercury decreased bile flow or changed the hepatic concentration of mercury of non-protein thiols. The possibility of the involvement of ligandin in the biliary excretion of methylmercury is discussed.

Animals↗
PubMed1979

Methylmercury poisoning in Canadian Indians--the elusive diagnosis.

A World Health Organization Expert Committee has concluded that symptoms of methylmercury poisoning may appear at blood concentrations of 200-500 ng Hg/ml. Blood levels in this range have been found in several Indian and Inuit communities in Canada. The syndrome of severe methylmercury poisoning (Hunter-Russell syndrome) is well described. However, diagnosis of less severe cases is difficult. This paper review the present situation in Canada. The problems of diagnosis currently being encountered are discussed and are illustrated by the case of an individual who had one of the highest blood concentrations (551 ng Hg/ml) ever described in fish-eating populations outside of the outbreaks in Minamata and Niigata in Japan. Although mercury concentrations in brain were estimated to have been in the "symptomatic" range at least once in the two years prior to his death, neurohistological examination was normal. Detailed examination by two teams of neurologists revealed effects that may be associated with methylmercury poisoning but a definitive diagnosis remained elusive.

Aged↗
PubMed1979

Tissue distribution of inhaled mercury vapor in acatalasemic mice.

Substantial differences were observed in the pattern of tissue deposition in normal versus acatalasemic mice after inhalation of radioactive mercury vapor. Liver deposition was approximately double and lung deposition approximately one-half the corresponding deposition in normal animals. These results lend further support to the idea that the hydrogen-peroxide catalase peroxidative pathway plays a role in the metabolism of inhaled mercury vapor.

Acatalasia↗
PubMed1979

Prenatal methylmercury poisoning. Clinical observations over five years.

Thirty-two infants prenatally exposed to methylmercury and their mothers were examined over a five-year period after the Iraqi methylmercury epidemic. Severity of poisoning in mothers was related to the peak mercury concentration in their hair and in the infants to the maximum concentration in maternal hair during pregnancy. In nine cases of cerebral palsy, methylmercury exposure occurred only during the last trimester. All infants except three (two were orphaned soon after birth and one was bottle-fed) were exposed postnatally via suckling. Whereas the mother's symptoms usually improved, the damage to the fetal nervous system appears to be permanent. Milder cases previously not identified in other studies are reported. The syndrome consists of varying degrees of developmental retardation in addition to exaggerated tendon reflexes and the pathologic extensor plantar reflex (minimal brain damage syndrome).

Abnormalities, Drug-Induced↗
PubMed1978

Enzymatic oxidation of mercury vapor by erythrocytes.

The formation of glutathione radicals, the evolution of nascent oxygen or the peroxidatic reaction with catalase complex I are considered as possible mechanisms for the oxidation of mercury vapor by red blood cells. To select among these, the uptake of atomic mercury by erythrocytes from different species was studied and related to their various activities of catalase (hydrogenperoxide : hydrogen-peroxide oxidoreductase, EC 1.11.1.6) and glutathione peroxidase (glutathione : hydrogen-peroxide oxidoreductase, EC 1.11.1.9). A slow and continuous infusion of diluted H2O2 was used to maintain steady concentrations of complex I. 1% red cell supsensions were found most suitable showing high rates of Hg uptake and yielding still enough cells for subsequent determinations. The results indicate that the oxidation of mercury depends upon the H2O2-generation rate and upon the specific acticity of red-cell catalase. The oxidation occurred in a range of the catalase-H2O2 reaction where the evolution of oxygen could be excluded. Compounds reacting with complex I were shown to be effective inhibitors of the mercury uptake. GSH-peroxidase did not participate in the oxidation but rather, was found to inhibit it by competing with catalase for hydrogen peroxide. These findings support the view that elemental mercury is oxidized in erythrocytes by a peroxidatic reaction with complex I only.

Animals↗
PubMed1978

Methylmercury poisoning in Iraqi children: clinical observations over two years.

The clinical features of 49 children who had eaten bread contaminated with methylmercury in rural Iraq were reviewed. Symptoms and signs relating to the nervous system--varying degrees of ataxia, weakness, and visual and sensory changes--dominated the clinical picture. The severity of poisoning was related to the blood mercury concentration, as was the degree of recovery. Follow-up over two years showed that children who had had mild or moderate poisoning slowly but steadily improved, some of them recovering normal function, though all had a residual generalized hyperreflexia. In some patients ataxia and motor weakness disappeared. Visual changes also improved, though less completely, and of 17 blind children, only five had recovered partial sight by the end of two years. Seven of the 18 children who suffered very severe poisoning were left physically and mentally incapacitated. The degree of clinical progress shown by these children was better than that shown by some other groups of patients, possibly because the poisoning was relatively acute and mercury consumption was stopped immediately after its effects had become obvious.

Adolescent↗
PubMed1978

Ethanol-increased exhalation of mercury in mice.

CBA/J mice injected three days beforehand with 203HgCl2 were given ethanol or water by gavage and placed in a chamber designed to collect exhaled mercury. Ethanol treatment led to an eight-fold increase of counts accumulated on a filter over a four-hour period, compared with water-treated mice. The mercury-collection apparatus tested for extracorporeal contribution of volatilised mercury indicated that the counts originated from the air exhaled by the mice.

Animals↗
PubMed1978

Exchange transfusion treatment of methylmercury-poisoned children.

Three children, ages 6 months, 13 months and 10 years were treated by exchange transfusions following exposure to methylmercury in the Iraq outbreak in 1971-72. Two had severe signs of poisoning and the other was clinically normal but had a high blood mercury concentration. Exchange transfusion resulted in clearance of mercury not only from blood but also from other tissues. The average amount of mercury removed in a two hour exchange was estimated as 6% of the body burden as compared to 1% of the body burden removed by normal excretion processes in 24 hours. No dramatic improvement in the clinical condition of the two poisoned patients occurred. Some improvement in motor power and function was observed during follow-up visits to their houses.

Child↗
PubMed1977

Organ mercury levels in infants with omphaloceles treated with organic mercurial antiseptic.

Samples of fresh and fixed tissues from infants with exomphalos treated by thiomersal application were analysed for mercury content. The results showed that thiomersal can induce blood and organ levels of organic mercury which are well in excess of the minimum toxic level in adults and fetuses. The analysis of fresh and fixed tissues must be carefully controlled against normal tissues in order to interpret mercury levels accurately.

Brain↗