Coagulation disorders following an accidental ingestion of cerium dioxide nanoparticles.

Clinically, acute cerium dioxide poisoning or damage is very rare. Here, the investigator reported a case about the patient who accidental ingested cerium dioxide nanoparticles during work shift. The patient recovered well after the treatment with removal of cerium and restoring coagulation factor activity. The author also reviewed relative literatures to discuss the potential mechanism of coagulation disorders following cerium dioxide nanoparticles ingestion. This case is the first report in the world about acute oral poisoning due to cerium dioxide nanoparticles, with the exact exposure concentration.

Methemoglobinemia by cerium nitrate poisoning.

Cerium nitrate is a topical antiseptic used with silver sulfadiazine (Flammacerium) for the treatment of serious burns. This topical agent can induce methemoglobinemia, but no cases have been reported in the recent literature. In this article, we present the case of a 16-year old girl, with third-degree burns over 95% of her body. After daily dressings of Flammacerium, on the sixth day she developed a bluish skin coloring. When tested for methemoglobinemia, levels of 31.8% were found. These returned to normal after classic treatment with Methylene blue.

The potencial role of rare earths in the pathogenesis of interstitial lung disease: a case report of movie projectionist as investigated by neutron activation analysis.

A 60-year-old male subject who worked as a movie projectionist and who was exposed for 12 years to rare earths (RE) containing dusts from cored arc light carbon electrodes was investigated. Chest X-ray films and pulmonary function tests showed an interstitial lung disease, emphysema and a severe obstructive impairment with marked decrease of carbon monoxide diffusion capacity. The histological examination of a transbronchial biopsy confirmed the diffuse interstitial lung fibrosis. Neutron activation analysis (NAA) of the biopsy showed concentrations of cerium (Ce), lanthanum (La), neodimium (Nd), samarium (Sm), terbium (Tb) and ytterbium (Yb) which were high compared to the corresponding elements in the transbronchial biopsies of 5 unexposed subjects as a control group. Thorium (Th) (which is generally present as an impurity of the RE compounds) was also determined in order to estimate the radiation dose in the lung of the worker. On the basis of the clinical observations, of the analytical results by neutron activation analysis of RE and of the presence of Th in the transbronchial biopsy, as well as of the differential diagnosis, which tended to exclude other occupational or non-occupational lung diseases, a relation between the observed interstitial lung fibrosis and occupational exposure to RE is highly probable.

Serum ornithine carbamoyltransferase (OCT) in rats poisoned with lanthanum, cerium and praseodymium.

Serum ornithine carbamoyltransferase (OCT) in rats poisoned with lanthanum, cerium and praseodymium. Acta Physiol. Pol., 1977, 28 (6): 589-594. The serum ornithine carbamoyltransferase in relation to doses of lanthanum, cerium and praseodymium, administered intravenously as chlorides, was investigated. A directly proportional relationship was found between the doses of these compounds and the serum enzyme level in rats. The lowest doses at which a rise in the serum OCT level occured were determined. They were: lanthanum - 0.75 mg/kg of body weight, cerium - 1.5 mg/kg, and praseodymium - 3 mh/kg. A decreasing toxicity of these elements with increasing value of atomic number was observed.

Differences in liver weight, mortality in cerium-treated mice and 144Ce levels in blood, liver, urine and faeces at various intervals after treatment with nafenopin and pregnenolone 16-alpha-carbonitrile (PCN).

Pretreatment with nafenopin and pregnenolone-16-alpha-carbonitrile (PCN) decreased the acute lethal toxicity in mice induced by cerium chloride (12 mg/kg resp. 15 mg/kg). Treatment with nafenopin and PCN increased the relative liver weight. More cerium accumulated in the liver of nafenopin- and PCN-treated animals than in controls during the first hours after injection. After 14 days the amount of cerium in the livers of nafenopin-treated animals was significantly higher. The concentration of cerium as a percentage of the injected dose calculated per mg liver was lower during the first day in the nafenopin group and higher in the PCN group than in the control group. After 6 days cerium concentration decreased significantly less in the livers of the nafenopin group. Cerium concentration in the blood was significantly lower in the nafenopin group during the first day. Only small amounts of the injected cerium were excreted in the urine, and no difference between treated and untreated animals was found. The amount of cerium excreted in faeces was somewhat smaller in the nafenopin-treated animals during the whole experiment.

Prevention by steroids of cerium hepatotoxicity.

In female rats, the lethality and hepatotoxicity of cerous chloride (CeCl3) were significantly altered by pretreatment with steroidal and nonsteroidal compounds (pregnenolone-16alpha-carbonitrile "PCN", dexamethasone, spironolactone, phenobarbital) that stimulate hepatic drug-metabolizine enzyme activity and by estradiol. PCN, estradiol, and dexamethasone considerably decreased hepatic triglycerides, but the latter steroid also greatly sensitized the animals to CeCl3 lethality. Spironolactone and phenobarbital similarly lowered the triglyceride level but not significantly. Light and electron microscopy indicated that the hepatocytic damage elicited by CeCl3 was decreased significantly by PCN, estradiol, and dexamethasone. The steroids may have altered the distribution and binding of the metal to the endoplasmic reticulum (er) thus protecting these membranes against the effect of cerium.