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Biomedical subjects

T W Clarkson

Publications and source records attributed to T W Clarkson.

162 records · Page 9Linked to original sources
PubMed1967

The transport of salt and water across isolated rat ileum. Evidence for at least two distinct pathways.

The flows of sodium, potassium, and chloride under electrical and chemical gradients and of salt and water in the presence of osmotic pressure gradients are described by phenomenological equations based on the thermodynamics of irreversible processes. The aim was to give the simplest possible description, that is to postulate the least number of active transport processes and the least number of separate pathways across the intestine. On this basis, the results were consistent with the following picture of the intestine: Two channels exist across this tissue, one allowing only passive transport of ions and the other only active. In the passive channel, the predominant resistance to ion flow is friction with the water in the channel. The electroosmotic flow indicates that the passive channel is lined with negative fixed charged groups having a surface charge density of 3000 esu cm-2. The values of the ion-water frictional coefficients, and the relationship between ionic concentrations and flows indicate that the passive channel is extracellular. The active channel behaves as two membranes in series, the first membrane being semipermeable but allowing active transport of sodium, and the second membrane being similar to the passive channel. Friction with the ions in the second "membrane" is the predominant resistance to water flow.

Animals↗
PubMed1966

Studies on the binding of mercury in tissue homogenates.

1. This paper describes an attempt to learn more about the binding of Hg(2+) to tissues at pharmacological concentrations of this metal. Other methods were not applicable to such low concentrations of mercury. 2. The method involved equilibrium dialysis of Hg(2+) against 1% homogenates of rat kidney or liver in the presence of penicillamine. Two classes of mercury-binding sites were observed, one class having a chemical affinity for mercury 100-fold greater than the other class. The binding capacities of the class of higher and lower affinity were respectively 1.0x10(-7) and 30x10(-7)mole of mercury/g. wet wt. of tissue. The same classes of binding sites were found in both liver and kidney homogenates. 3. The binding sites of both classes reacted with only one valency of Hg(2+), the other valency forming a bond with penicillamine. Thus the total binding capacities of both classes are equivalent to 50% of the total reactive protein-bound thiol groups in the homogenate. 4. The results eliminate three possible mechanisms for the preferential accumulation of mercury by kidney. They support the idea that the permeability changes in kidney cells resulting in diuresis are similar to the permeability changes produced on the membranes of other mammalian cell species by mercury.

Animals↗
PubMedDate not supplied

The metabolism of arsenite and arsenate by the rat.

Differences in distribution and metabolism of arsenite and arsenate were studied in rats and in rat liver and kidney slices and hepatocytes. Five minutes after i.v. administration of 4.8 nmol arsenite or arsenate to male Sprague-Dawley rats, blood levels of arsenic were only 10 percent of the initial dose. Blood arsenic levels then rose: by 4 hours about 67 percent of the initial dose of arsenite and 28 percent of the initial dose of arsenate were in the blood compartment. The predominant form of arsenic in the RBC was dimethylarsinic acid (DMA). Arsenite was rapidly distributed to both liver and kidney; arsenate was rapidly distributed to kidney only. After 4 hours of exposure to arsenite, liver slices had taken up six times more arsenic and kidney slices two times more arsenic than after exposure to arsenate. Isolated hepatocytes took up as much as 20 times more arsenic after arsenite exposure. DMA was found in the medium of the liver slices and hepatocytes exposed to arsenite, but very little DMA was found in the medium of the arsenate-exposed liver slices and hepatocytes. However, five times more DMA was found in the medium of the kidney slices exposed to arsenate than in the medium of the liver slices. Phosphate inhibited uptake and metabolism of arsenate by kidney slices. These studies indicate that inorganic arsenic is rapidly taken up by liver and kidney and methylated. Arsenite is methylated by both organs, whereas arsenate may be methylated by kidney only.

Animals↗
PubMedDate not supplied

Clearance of mercury (HG-197, HG-203) vapor inhaled by human subjects.

Five human subjects inhaled a mixture of stable and radioactive mercury vapor for periods of 14 to 24 minutes. The subjects retained an average of 74% of that inhaled. Evidence is submitted to show that the retention occurred almost entirely in the alveoli. For 3 days after exposure, the exhaled breath was passed at intervals through activated charcoal traps for sampling periods of 10 to 35 minutes. The data indicated that an average of 7% of the retained mercury was lost in the expired breath, with a half time of 18 hours. Examination of the subjects in a whole body counter yielded average half times for mercury clearance from different parts of the body as follows: lung, 1.7 days; head, 21 days; kidney region, 64 days; chest, 43 days; and whole body, 58 days.

Adult↗
PubMedDate not supplied

Radioactive mercury distribution in biological fluids and excretion in human subjects after inhalation of mercury vapor.

The distribution of mercury in red blood cells (RBCs) and plasma, and its excretion in urine and feces are described in five human subjects during the first 7 days following inhalation of radioactive mercury vapor. A major portion (98%) of radioactive mercury in whole blood is initially accumulated in the RBCs and is transferred partly to the plasma compartment until the ratio of mercury in RBCs to plasma is about 2 within 20 hr. The cumulative urinary and fecal excretion of mercury for 7 days is about 11.6% of the retained dose, and is closely related to the percent decline in body burden of mercury. There is little correlation between either the urinary excretion and plasma radioactivity of mercury, or the specific activities of urine and plasma mercury, suggesting a mechanism other than a direct glomercular filtration involved in the urinary excretion of recently exposed mercury. These studies suggest that blood mercury levels can be used as an index of recent exposure, while urinary levels may be an index of renal concentration of mercury. Howver, there is no reliable index for mercury concentration in the brain.

Adult↗
PubMedDate not supplied

A nonoccupational outbreak of inorganic mercury vapor poisoning.

An outbreak of inorganic mercury vapor poisoning involving 12 people occurred in a trailer park in Mississippi in 1973-74. For information concerning levels of mercury in hair and blood of humans with short-term exposures, these individuals were observed for as long as 10 months after the end of their exposures, and the amount of mercury in their blood and scalp hair was serially measured. Specimens were also obtained from nonexposed individuals in the trailer park. Inorganic mercury was measured in 1-cm segments of hair samples obtained both 6 and 9 months after termination of exposure. Over a 3-month period, the peak amount of inorganic mercury per gram of hair shifted in position from 7 cm to 13 cm from the scalp. The average mercury concentration in newly formed hair (the 4 cm of hair closest to the scalp) decreased fourfold over the same time period. Surface contamination of exposed hair by exogenous mercury also occurred. Levels of inorganic mercury in blood from exposed individuals ranged from 183 to 620 ng/ml and fell to levels similar to those of controls 4 to 6 months after ending exposure. The source of the outbreak was metallic mercury spilled on rugs. Attempts to remove the mercury failed and actually dispersed the metal over a larger surface area. Air mercury levels as high as 1.0 mg/m3 of air were found in one of the contaminated house trailers. Rugs or carpets contaminated with metallic mercury are a significant health risk.

Accidents, Home↗
PubMedDate not supplied

The relationship between blood levels and dose of methylmercury in man.

The kinetics of blood deposition and clearance of methylmercury were measured in volunteers given a single meal of fish containing 18 to 22 microgram mercury/kg body weight. Peak blood concentrations were achieved within 4 to 14 hr. Disappearance from blood was biphasic, with average half-times of 7.6 hr and 52 days, respectively. The fraction of the dose deposited in the blood volume after completion of tissue distribution was 5.9%. Blood concentrations of total mercury reached as high as 60 ng mercury/ml, whereas inorganic mercury did not exceed 2 ng mercury/ml. The average red blood cell to plasma concentration ratio was 21 and the hair to blood ratio was 292. The kinetic parameters relating to blood deposition and clearance were used to calculate the expected relationship between average long-term daily intake of methylmercury and steady state blood concentration.

Adult↗
PubMedDate not supplied

Interrelationships of blood and hair mercury concentrations in a North American population exposed to methylmercury.

Samples of blood and head hair were analyzed for organic and inorganic mercury from a population which consumed large amounts of fish contaminated with methylmercury. Mercury levels in newly formed hair were found to reflect those in blood with the concentration in hair being approximately 300 times that in blood. Organic and inorganic mercury levels were linearly related in both hair and blood samples, with a mean inorganic/organic ration of 0.05 in blood and 0.21 in hair, but individual differences were found to exist. In addition, the total mercury concentration and inorganic/organic ratio in hair remained constant with time. Thus, longitudinal analysis of hair samples can provide a simple and accurate method of monitoring continuing exposure and an estimation of peak blood levels months to years after exposure.

Animals↗
PubMedDate not supplied

Methylmercury in populations eating large quantities of marine fish.

A Peruvian population was identified that was chronically exposed to methylmercury from the long-term consumption of ocean fish. The weekly fish intake averaged 10.1 kg per average family of 6.2 persons. Blood methylmercury concentrations ranged from 11 to 275 ng/ml, with a mean of 82 ng/ml. Paresthesias were reported by 29.5% of the population. In contrast, a nearby control population had a mean weekly fish consumption of 1.9 kg per average family of 6.4 persons. Their blood methylmercury levels were 3.3-25.1 ng/ml, with a mean of 9.9 ng/ml. Paresthesias were reported by 49.5% of this control group. No individual was identified with symptoms or signs that could be attributed to methylmercury intoxication.

Adolescent↗
PubMedDate not supplied

Percutaneous absorption of mercury vapor by man.

Five volunteer male subjects who were 24 to 78 y of age exposed the skin of their forearm to mercury vapor (203Hg) at concentrations of 0.88-2.14 ng/cm3 for periods of 27-43 min. Approximately 216 to 844 ng was taken up by the skin at rates of 0.0101 to 0.0402 ng Hg per cm2 per min per ng Hg per cm3 air. About half of the mercury taken up was shed by desquamation of epidermal cells during several weeks. The remainder diffused into the general circulation and could be measured as systemic mercury. When the total skin area (of which the forearm skin was assumed to be representative) was compared to the lung as a route of entry for mercury vapor at the same concentration, the rate of uptake was estimated to be 2.2% of the rate of uptake by the lung. A model is proposed that describes the growth and loss of skin-derived systemic mercury.

Adult↗
PubMedDate not supplied

Organic mercury exposure from fungicide-contaminated eggs.

During a period of 50 to 55 days from early January to March 2, 1979, 14 members of an extended family in Yakima, Washington, ate eggs contaminated with organic mercury. Seed grain which had been treated with a mercurial fungicide and fed to chickens in a home flock was the source of exposure. Blood mercury levels in family members ranged from 0.9 to 20.2 ppb and correlated positively with average daily egg consumption (r = 0.92). There were no symptoms or physical signs of organic mercury intoxication. Prompt confiscation of the contaminated grain, eggs, and chicken flock terminated the exposure and may have prevented the development of serious illness.

Adolescent↗