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T Norseth

Publications and source records attributed to T Norseth.

At least 37 records · Page 2Linked to original sources
PubMed1983

Cancer incidence in the rubber industry in Norway.

Cancer incidence was studied among 2,448 male rubber workers employed for 18 months or more with at least eight years of observation time. A suggested increased risk of bladder cancer, lymphoma, and leukemia was found in the footwear department; the number of observed to expected cases was 4/2.81, 5/2.26, and 4/1.76, respectively. An unexpected increased risk of pancreatic cancer was found for the maintenance-workshop department, the observed to expected numbers being 6/0.90.

Humans↗
PubMed1982

Uptake of chromium by rat liver mitochondria.

Isolated rat liver mitochondria rapidly accumulate chromate (1.2 microM 51CrO4(2-)) to about 0.25-0.30 nmol Cr/mg protein. The relative uptake decreases with increasing chromate doses. Chromate uptake decreases when pH is raised from 7.0 to 7.5.N-ethylmaleimide (0.25 mM) and butylmalonate (5 mM) inhibit chromate uptake to 70% and 30% of control values, respectively, whereas mersalyl (40 nmol/mg protein) causes an inhibition of greater than 95%. Both sulphate and phosphate decrease mitochondrial chromate uptake, the former being more effective in lower doses (5 mM). These results indicate that transport of chromate is mediated both on the dicarboxylate and the phosphate carrier. The extensive mitochondrial chromium accumulation can be explained by trapping of chromium, probably by reduction of chromate to the trivalent form, within the mitochondria. Release of chromium after chromate loading was seen after 15 min. Added after chromate loading, mersalyl partly prevents this release. Trivalent chromium as 51CrCl3 is taken up to a much lower degree than hexavalent chromium as 51CrO4(2-). The presence of glutathione (5 mM) reduces the uptake both of 51Cr-III and 51Cr-VI, indicating extramitochondrial reduction of Cr-VI to Cr-III and subsequent binding to GSH.

Animals↗
PubMed1982

Uptake of 51Cr-chromate by human erythrocytes-a role of glutathione.

Hexavalent chromium (Cr-VI), as Na2CrO4 in an aqueous solution, was reduced rapidly ot the trivalent form (Cr-III) in the presence of glutathione, GSH (0.3-3.0 mM). Such GSH-dependent reduction Cr-VI can take place in the cytosolic space of Cr-VI-exposed cells, since GSH is found in reactive concentrations in this compartment. The reduction makes chromium essentially impermeable through the cell membrane, explaining the observation that Cr-VI, when added to red cell suspensions, is bound quantitatively intracellularly after a few hours. Diethylmaleate conjugation of the SH-group of the intracellular GSH preventing the oxidation to GSSG, lowered the chromium-uptake significantly, showing that reduced GSH plays a role for the chromium binding. In healthy red cells chromium is partially bound to haemoglobin and partially to small molecular weight substances, probably in the trivalent form. This intracellular chromium cannot be removed to the extracellular space by addition of chelating agents as long as the cell membrane is intact.

Chromates↗
PubMed1982

Biliary excretion of chromium in the rat: a role of glutathione.

The relative amount of chromium excreted in rat bile after injection of Cr-III is much less than after injection of Cr-VI, about 0.1% and from 6-8% during 5 hours respectively, for corresponding dose levels. The liver to bile ratio was 50-100 for Cr-III injection, for Cr-VI the ratio was 2-3. With doses up to 18 mumol Cr/kg, only Cr-III was found in bile even after injection of Cr-VI. Glutathione depletion of the liver with cyclohexene oxide decreased chromium excretion in bile. Such treatment also decreased the reduction of Cr-VI to Cr-III in the liver cell as only Cr-VI was found in bile. A different distribution of Cr-III in the liver dependent on whether derived from Cr-VI or taken up by the liver as such must be assumed. Taking into account the usual low penetration of biological membranes by Cr-III, a possible active transport mechanism or a specific diffusable Cr-III compound must be postulated.

Animals↗
PubMed1981

Amphibole fibers in a taconite mine and in the lungs of the miners.

Fibers of the amphibole mineral series have been demonstrated in the dust from an open taconite ore mine. Though the total dust levels in some places are high, exposures to fibers are below one fiber/cc. The energy dispersive X-ray spectra of the amphibole fibers correspond to those of cummingtonite-grunerite, hornblende, or actinolite. The same type and size distribution of fibers were found during post mortem analyses of lung tissue from two previously exposed miners. The pathological examination revealed an undifferentiated small cell carcinoma of left lung as well as pulmonary fibrosis in one of the cases. In the second case a poorly differentiated squamous cell carcinoma of left lung was found along with silicosis.

Asbestos↗
PubMed1981

The carcinogenicity of chromium.

The carcinogenicity of chromium compounds is reviewed with specific attention to the gaps in knowledge for risk estimation and research needs. The most important problems at present are whether trivalent chromium compounds cause cancer, and whether there is a difference in cancer causing effects between the soluble and the slightly soluble hexavalent compounds in the practical exposure situation. Dose estimates for risk estimation based on epidemiological investigations are also lacking. Present evidence indicates that the trivalent chromium compounds do not cause cancer although high concentrations in some in vitro systems have shown genetic toxicity. Hexavalent chromium compounds cause cancer in humans, in experimental animals and exert genetic toxicity in bacteria and in mammalian cells in vitro. Epidemiological evidence and animal experiments indicate that the slightly soluble hexavalent salts are the most potent carcinogens, but proper identification and characterization of exposure patterns in epidemiological work are lacking. Workers also tend to have mixed exposures. Soluble and slightly soluble salts are equally potent genotoxic agents in vitro. Further work for establishing dose estimates for risk evaluation in epidemiological work is important. In vitro systems should be applied for further identification of the mechanism of the carcinogenic effects, and animal experiments are urgent for comparison of the carcinogenic potency of the different hexavalent salts. Hexavalent chromium salts must be regarded as established carcinogens, and proper action should be taken in all industries with regard to such exposure. At present the carcinogenic risk to the general population caused by chromium compounds seems to be negligible, chromium in cigarettes, however, is an uncertainty in this respect. The amount of chromium and the type of chromium compounds inhaled from cigarettes is not known.

Animals↗
PubMed1979

The effect of selenium on the biliary excretion and organ distribution of mercury in the rat after exposure to methyl mercuric chloride.

The influence of selenium compounds on the biliary excretion and the organ distribution of mercury after injection of methyl mercuric chloride (4 mumol/kg) have been tested. Selenite, seleno-di-N-acetylglycine and seleno-methionine strongly inhibited the biliary excretion of mercury. Selenite even in a molar dose of 1/40 of the methyl mercury dose inhibited the biliary excretion of mercury. The less toxic seleno-di-N-acetylglycine was needed in larger molar doses and did not act as rapidly as selenite. Biliary excreted methyl mercury is known to be partly reabsorbed in the gut. Subsequently a part of it is deposited in the kidneys since drainage of the bile lowered the kidney content of mercury. Rats given selenium compounds in combination with bile drainage showed further reduction of the kidney mercury content than bile duct drainage alone. Thus the demonstrated lowering effect of selenium compounds on the kidney mercury content cannot be completely explained by an inhibition of biliary excretion of mercury. The mercury concentration in the brain was increased by the selenium compounds; the effect being dependent of the selenium dose reaching a maximum at an equimolar selenite--to methyl mercury dose ratio. The mechanisms by which selenium influences the methyl mercury kinetics are discussed.

Animals↗