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M Piscator

Publications and source records attributed to M Piscator.

At least 19 recordsLinked to original sources
PubMed1991

Early detection of tubular dysfunction.

The determination of low-molecular-weight proteins in urine as a tool for early detection of damage to the proximal tubules is briefly discussed. Beta 2-microglobulin, retinol-binding protein and alpha 1-microglobulin are at present the most widely used markers for tubular dysfunction. The determination of beta 2-microglobulin has earlier been the method of choice, but due to its instability at low pH there are certain disadvantages. Available data indicate that alpha 1-microglobulin may replace beta 2-microglobulin for screening purposes. The low-molecular-weight proteins are at present the best markers for early detection of tubular dysfunction; other constituents are not as well suited for this, even if the determination of urine enzymes has its supporters.

Albuminuria↗
PubMed1989

Markers of tubular dysfunction.

Since the first description of tubular proteinuria in 1958, much progress has been made with regard to diagnostic means for detecting small changes in the function of the proximal tubule. Small increases in the excretion of low-molecular-weight proteins can now be determined with great accuracy. Determination of total protein is an economic way of screening large populations but does not give specific information on the type of damage. Determinations of glucose, phosphate and amino acids are relatively insensitive methods, since their excretion is also dependent on diet and nutritional status. Determination of high-molecular-weight enzymes released from damaged tubular cells may be of use for studies of acute as well as chronic effects of nephrotoxic agents, but more data are needed.

Biomarkers↗
PubMed1985

Dietary exposure to cadmium and health effects: impact of environmental changes.

Cadmium exposure, metabolism, and effects are described especially in relation to dietary intakes. Data on dietary intakes in several countries have been complied from studies using the duplicate diet method or fecal analysis. These two methods seem to give more accurate data than estimates based on cadmium concentrations in food classes and food consumption (composite method). The present data on absorption and retention of ingested cadmium indicate that normally less than 5% is ingested, but absorption may increase in women who have iron deficiency. Earlier estimates of the critical concentration in renal cortex being about 200 mg/kg wet weight still seem to be valid. New information is available on present renal levels and their distribution in the general population. The present margin of safety with regard to risk for renal effects is small. To predict future health risks from increases in dietary cadmium due to environmental changes such as acid deposition, it is necessary that the models used are based on correct assumptions. Of interest are the distributions of dietary intake, gastrointestinal absorption, and renal cadmium concentrations. These distributions are normal or lognormal, and since standard deviations are used when estimating risks, it is of paramount importance that the standard deviations are estimated as accurately as possible. At present it is not possible to quantify the effects attributed to acid rain only; account must be also be taken of cadmium added to, e.g., soil by use of sewage sludge and other fertilizers. In addition to risks to human health, cadmium also poses a threat to horses, which generally have renal cadmium concentrations several times higher than adult humans. It is recommended that horses should be monitored in areas when acid deposition is high. Such monitoring might provide valuable information about impact of acid rain.

Age Factors↗
PubMed1984

Long-term observations on tubular and glomerular function in cadmium-exposed persons.

Four groups of cadmium-exposed persons, from different workplaces and with different types of exposure, have been followed for periods of 9-20 years. In one group the total observation time is over 30 years, since they were included in Friberg's original study. The studies include determination of inulin or creatinine clearance, protein excretion and specific indicators of renal tubular dysfunction. The results indicate that once tubular dysfunction is established, it is irreversible, even when it is minor. In some persons it was noted that the development of renal dysfunction seemed to be a multistage process. The initial stage is characterized by an increased excretion of low molecular weight proteins like beta 2-microglobulin and ribonuclease. After a period of several years with no or low exposure, there was a relatively sharp increase in excretion of total proteins and albumin and a decrease in glomerular filtration rate. This is interpreted as being the result of further increases in renal concentration of cadmium and in spread of cadmium along the tubules. Metallothionein absorption in the tubules, its catabolism and synthesis must play an important role for the development and progress of the tubular dysfunction. It was not possible to show that a decrease in glomerular filtration rate occurs before low molecular weight proteinuria.

Aged↗
PubMed1984

Metallothionein in rabbit kidneys preserved for transplantation.

Thirteen rabbits were given repeated cadmium injections to achieve cadmium concentrations in kidney cortex ranging from 0.05 to 1 mmole Cd/kg wet weight. Another four animals served as controls. One kidney from each animal was frozen directly to -70 degrees C whereas the other kidney was kept for 24 hr at +4 degrees C in a preservative (Sachs' solution) to simulate conditions for preservation of human donor kidneys before transplantation. Protein binding of cadmium, zinc and copper in kidney homogenates and the concentration of metallothionein (MT) were measured in the kidney that was frozen directly and in the kidney that had been preserved. No gross differences in either the protein binding of cadmium, zinc and copper or in the MT content were seen between the directly frozen and preserved kidneys from the same animal. This indicates that MT is not rapidly broken down in rabbit kidneys which have been preserved similarly to human donor kidneys for 24 hr in a standard preservative solution prior to a transplantation.

Animals↗
PubMed1983

Cadmium exposure from smoking cigarettes: variations with time and country where purchased.

Cadmium has been determined in 26 brands of cigarettes purchased in eight different countries throughout the world and in 16 different samples of cigarettes produced in Sweden between 1918 and 1968. In addition the amount of cadmium released from smoking one cigarette to the particulate phase collected from a smoking simulation machine, corresponding to the amount actually inhaled by a smoker, has been determined. The cadmium concentration in different brands of cigarettes ranged from 0.19 to 3.0 micrograms Cd/g dry wt, with a general tendency toward lower values in cigarettes from developing countries. No systematic change in the cadmium concentration of cigarettes with time could be revealed. The amount of cadmium inhaled from smoking one cigarette containing about 1.7 microgram Cd was estimated to be 0.14 to 0.19 microgram, corresponding to about 10% of the total cadmium content in the cigarette.

Cadmium↗
PubMed1983

Cadmium in blood and urine related to present and past exposure. A study of workers in an alkaline battery factory.

Blood and urinary cadmium concentrations together with cadmium in air concentrations from the breathing zone of 18 male workers in an alkaline battery factory were determined at regular intervals for 11 consecutive weeks. Nine of the workers examined were smokers and nine non-smokers. Smokers and non-smokers did not differ in age or years of employment. Cadmium in air concentrations varied, but no definite trend was observed. The concentrations of cadmium in the blood and urine were found to be stable. Exposure to airborne cadmium was identical for smokers and non-smokers but average cadmium concentrations in the blood and urine of smokers were approximately twice as high as those in non-smokers. For the whole group, urinary cadmium was significantly correlated with years of employment, but no correlation was found between blood cadmium concentrations and exposure. For non-smokers, the correlation between cadmium in blood and years of employment was statistically significant (p less than 0.001). This finding indicated that blood concentrations of cadmium reflect body burden in non-smokers at current low exposure levels.

Adult↗
PubMed1981

Beta 2-microglobulin levels in serum and urine of cadmium exposed rabbits.

Male rabbits were exposed to cadmium during 16 weeks by subcutaneous injections of either 0.25 mg or 0.5 md Cd as cadmium chloride per kg body weight 3 times per week. beta 2-microglobulin (beta 2-m) and creatinine in serum, cadmium in blood, as well as total protein, creatinine, beta 2-m and cadmium in urine were determined before exposure and after 3 and 7 weeks of exposure. Measurements were also made at 19 weeks, 3 weeks after the last exposure. During exposure, there was a slight increase in the serum beta 2-m/creatinine ratio among rabbits with the highest exposure, while no effect of the cadmium burden could be observed once exposure had ceased. Urinary excretion of beta 2-m was related to urinary pH, which appeared to be the case also for excretion of total protein. In the high exposure group, a significant increase in urinary beta 2-m excretion, indicative of renal tubular dysfunction was seen after 7 weeks of exposure. This was, however, not related to serum beta 2-m levels. It was concluded that before renal damage has occurred even heavy cadmium exposure has very little influence on serum beta 2-m levels.

Animals↗
PubMed1981

Role of cadmium in carcinogenesis with special reference to cancer of the prostate.

It has been shown in animal experiments that injections of large amounts of cadmium cause sarcoma at injection sites or testicular damage and eventually testicular tumors. Long-term exposure with small doses of cadmium has not caused testicular or prostatic tumors in experimental animals. Epidemiological studies on cadmium-exposed workers have shown excess deaths due to prostatic cancer in at least three independent investigations. All reported cases probably had considerable exposure decades ago, but there are not enough data to permit any dose-response calculations. The general epidemiology of prostatic cancer was not taken into account in any of the studies. A review of recent literature on epidemiology of prostatic cancer has revealed some basic facts. Small latent prostatic cancer has been shown to be as common in areas with low mortality from prostatic cancer as in areas with high mortality. In the U.S. the black population has a much higher death rate from prostatic cancer than the white population. Marital status has also been implied as a factor in the development of prostatic cancer. Black populations in Africa have much lower death rates than blacks in the U.S., which may depend on large differences in dietary habits. Thus racial, sexual and nutritional factors might be important for the development of prostatic cancer, since they may influence hormonal status. Cadmium concentrations in testes and prostate increase during heavy exposure, and it has been shown that testosterone synthesis will decrease in cadmium-exposed animals. Excessive exposure may interfere with the zinc/hormone relationship in the prostate, which could be a possible explanation for the development of prostatic cancer in heavily exposed individuals. Direct action of cadmium on the cells is not likely, nor is it probable that low level exposure to cadmium can be a causative factor for prostatic cancer.

Animals↗
PubMed1979

Pulmonary and gastrointestinal exposure to cadmium oxide dust in a battery factory.

The elimination of cadmium in feces was studied in a group of 15 male workers exposed to cadmium oxide dust in a nickel-cadmium battery factory. The elimination of cadmium in feces was on the average 619 and 268 microgram/day in seven smokers and eight nonsmokers, respectively. The corresponding ranges were 97-2577 and 31-1102 microgram/day. The cadmium concentrations in blood were significantly higher in smokers than in nonsmokers, both before and after one month of vacation. Among the smokers there was a significant decrease in the cadmium concentrations during the vacation period, but not among the nonsmokers. It was estimated that cadmium naturally occurring in food and cigarettes, cadmium excreted from the gastrointestinal tract, and cadmium transported from the lungs by mucocillary clearance to the gastrointestinal tract only could explain up to 100 microgram of the cadmium in the feces. Since even among some nonsmokers much higher values for fecal cadmium were recorded, this was interpreted as being the result of ingestion of cadmium from contaminated hands and other body surfaces. Among the smokers, direct oral contact with contaminated cigarettes or pipes is an additional factor; the smokers also inhale cadmium in the tobacco smoke from contaminated cigarettes. Part of that cadmium is transferred to the gastrointestinal tract by mucociliary clearance and also adds to the fecal cadmium.

Adult↗