Pulmonary toxicity of indium arsenide and arsenic selenide following repeated intratracheal instillations to the lungs of hamsters

Chronic toxicity of indium arsenide (InAs) and arsenic selenide (As₂Se₃) was studied in male Syrian golden hamsters which received InAs or As₂Se₃ particles, each containing a total dose of 7.5 mg of arsenic, by intratracheal instillations once a week for 15 weeks. As a control, hamsters were treated with the vehicle, phosphate buffer solution. During their total lifespan, the cumulative body weight gain of the hamsters in the InAs group was suppressed significantly compared with that in the control group, but not in the As₂Se₃ group when compared with that in the control group. However, the survival rate for the InAs group was significantly higher compared with the control group, but not for the As₂Se₃ group when compared with the control group. During the animals' total lifespan, one lung adenoma was seen in the 27 hamsters in the InAs group and one lung adenoma in the 23 hamsters in the control group. No tumors of the lung were observed in the As₂Se₃ group. Malignant tumors outside the lung appeared in four hamsters in the InAs group and in two in the As₂Se₃ group. No non-lung malignant tumours were seen in the control group. Total tumor incidence rates were 25.9% (7/27) in the InAs group, 10.3% (3/29) in the As₂Se₃ group and 8.7% (2/23) in the control group. There were therefore no significant differences in tumor incidence between the InAs or the As₂Se₃ group, and the control group. Regarding histopathological findings in the lung, incidence rates of proteinosis-like lesions, pneumonia, metaplastic ossification and emphysema were seen only in the InAs group, and alveolar or bronchiolar cell hyperplasia observed in both the InAs and the As₂Se₃ groups were at significantly higher rates than those in the control group. From these results, it was concluded that InAs and As₂Se₃ particles could induce pulmonary toxicity when instilled intratracheally into hamsters. A great deal of attention should be paid to the toxicity of both InAs and As₂Se₃, even though in this study the adverse health effects of As₂Se₃ appeared to be less than those of InAs.     

Comparative chronic toxicity,including tumorigenicity,of gallium arsenide and arsenic trioxide intratracheally instilled into hamsters

Chronic toxicity, including tumorigenicity, of gallium arsenide (GaAs) and arsenic trioxide (As₂O₃) were studied using Syrian golden hamsters given intermittent intratracheal instillations. GaAs particles (0.25 mg × 15 times/animal) were likely to produce relatively severe lung damage and the survival of the animals was shortened significantly compared with a control group. The tumor incidence of each group examined was GaAs (3.3%), As₂O₃ (3.3%) respectively, at a dose of 3.75 mg total metal given during 15 weeks. In this experiment, both arsenic trioxide and gallium arsenide had no apparent carcinogenicity or tumorigenicity.     

Conversion of arsenite and arsenate to methylarsenic and dimethylarsenic compounds by homogenates prepared from livers and kidneys of rats and mice

Pooled livers and pooled kidneys from rats or mice were homogenized and spiked with arsenite or arsenate in the concentration range 1.3–20 μmol dm^?3. Methylarsenic and dimethylarsenic compounds were determined by the hydride generation technique in the homogenates after a 90 min incubation at 37°C. The rat homogenates methylated arsenite and arsenate more efficiently than the mouse homogenates. Monomethylated arsenic was present in larger amounts than dimethylated arsenic in the rat homogenates. In the absence of reduced glutathione (GSH), no methylation occurred. Addition of GSH promoted monomethylation and dimethylation, whereas dithiothreitol and mercaptoethanol (10 mmol dm^?3) fostered only monomethylation. The amounts of monomethylated arsenic in the rat liver homogenates increased with increasing arsenite concentration (1.3–20 μmol dm^?3) however, the percentage of arsenic that had been methylated decreased. A similar trend, but with much less monomethylarsenic formed, was observed for arsenate-spiked homogenates. Rat kidney homogenates methylated arsenite and arsenate to a much smaller extent than rat liver homogenates. The K_m values for the monomethylation in rat liver homogenates were found to be 5.3 μmol dm^?3 for arsenite and 59 μmol dm^?3 for arsenate.     

Tunable te-CO2 laser-pumped formaldehyde far-infrared lasers: Offsets, assignment, and superfluorescence

Sixty and three absorption transitions in D₂CO and H₂CO, respectively, have produced a number of far infrared laser lines when they are pumped by an etalon-tuned TE-CO₂ laser. Almost all the absorption transitions pumped previously by a free runing TE-CO₂ laser have been efficiently pumped by the etalon tuned CO₂ laser and found to have offset within ±500 MHz from the line-center of the relevant CO₂ pump lines. 22 (1) absorption and 63 (4) emission lines of D₂CO (H₂CO) are assigned. Some of these lines have generated superfluorescence. In paticular, the D₂CO 319-m line pumped by CO₂-9P(32) delivered an output energy of approximately one half that of the well-known D₂O 66-m. It is shown that a large electric dipole moment and an appreciable amount of fractional population in the lower level of the pump transition of this line are responsible to the superfluorescence.     

Glutathione and methylation of inorganic arsenic in hamsters

The effect of giutathione (GSH) concentrations in livers and kidneys of hamsters on the toxicity and methylation of arsenite in these animals was studied. No significant changes in hepatic and renal GSH concentrations were observed after a single arsenite administration (5 mg As kg^?1, p.o.). When buthionine sulfoximine (BSO), an inhibitor of GSH synthesis, was given (4 mmol kg^?1, i.p.) two hours before administration of arsenite, hepatic and renal GSH concentrations were more severely and persistently depressed than in the case of BSO administration not followed by arsenite. Hamsters treated with BSO plus arsenite suffered from severe nephrotoxicity (acute renal failure) characterized by increases in plasma creatinine and urea nitrogen and by proximal tubular necrosis. Concurrently, transient hepatotoxicity was observed in the BSO plus arsenite group. Neither arsenite alone nor BSO alone produced liver or kidney injury. The BSO plus arsenite-treated animals excreted in the urine only 3.5% of the arsenic dose during the 72 h period after administration of arsenite, probably because of a decrease in urine volume caused by kidney injury, whereas the arsenite-only group excreted 27%. In addition, BSO pretreatment influenced the relative proportion of arsenic metabolites excreted in the urine during the first 24 h after administration. Urinary metabolites in the BSO plus arsenite group were predominantly inorganic arsenic. These results suggest that GSH provides protection against arsenic toxicity.