Effects of Intratracheally Administered Indium Phosphide on Male Fischer 344 Rats

Takamoto UEMURA; Kenichi ODA; Kazuyuki OMAE; Toru TAKEBAYASHI; Tetsuo NOMIYAMA; Chizuru ISHIZUKA; Kanae HOSODA; Haruhiko SAKURAI; Kazuto YAMAZAKI; Isamu KABE

doi:10.1539/joh.39.205

Takamoto UEMURA, Kenichi ODA, Kazuyuki OMAE, Toru TAKEBAYASHI, Tetsuo NOMIYAMA, Chizuru ISHIZUKA, Kanae HOSODA, Haruhiko SAKURAI, Kazuto YAMAZAKI, Isamu KABE

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Keywords: Indium phosphide, Semiconductor, Intratracheal administration, BALF (Bronchoalveolar lavage fluid), Toxicity, Rats

JOURNAL FREE ACCESS

1997 Volume 39 Issue 3 Pages 205-210

DOI https://doi.org/10.1539/joh.39.205

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Published: 1997 Received: August 19, 1996 Available on J-STAGE: April 07, 2006 Accepted: December 18, 1996 Advance online publication: - Revised: -
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Date of correction: April 07, 2006 Reason for correction: - Correction: ABSTRACT Details: Wrong : Effects of Intratracheally Administered Indium Phosphide on Male Fischer 344 Rats: Takamoto UEMURA, et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University—Objective—To examine the effects of intratracheally administered indium phosphide (InP) and distribution of indium on male Fischer 344 rats. Materials and methods—Rats were intratracheally given 0, 1, 10 or 100 mg/kg of InP with a mean diameter of 0.8μm and observed for 1 and 7 days. The bronchoalveolar lavage fluid (BALF) was examined biochemically and cytologically. Serum biochemical, hematological and histopathological examinations were done, and the indium concentration in organs and serum was determined. Findings—The number of neutrophils in BALF remarkably increased in a dose-effect manner 1 and 7 days after administration and InP particles were phagocytized in the macrophages. Total protein (TP), lactate dehydrogenase (LDH), total phospholipid (TPL) and total cholesterol (T-Cho) in BALF showed a clear dose-effect relationship 7 days after administration. Indium was detected in the liver and spleen and increased in a dose-related manner on the next day and 7 days after administration. Serum indium was detected in the group given more than 10 mg/kg but did not reveal a dose relationship. Histopathological examination of the lungs showed phagocytized InP particles in the macrophages and the migration of neutrophiles in the alveoli. InP particles remained in the bronchioles and alveoli until 7 days after. No histopathological changes were detected in the liver or spleen . A hematological study did not reveal significant findings. Interpretation/—Intratracheally administered InP particles cause pulmonary inflammation and those particles remain in the lower airways for at least 7 days. Phagocytosis of macrophages may contribute to their disposal and distribution to the liver and spleen. Further study is required with particles with a lower toxic activity than InP and with the same particle size as the InP used in this study, to clarify their specific toxicity. Simultaneously longer observation is needed to assess toxicity in the other organs after distribution.
Right : Effects of Intratracheally Administered Indium Phosphide on Male Fischer 344 Rats: Takamoto UEMURA, et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University—Objective—To examine the effects of intratracheally administered indium phosphide (InP) and distribution of indium on male Fischer 344 rats. Materials and methods—Rats were intratracheally given 0, 1, 10 or 100 mg/kg of InP with a mean diameter of 0.8μm and observed for 1 and 7 days. The bronchoalveolar lavage fluid (BALF) was examined biochemically and cytologically. Serum biochemical, hematological and histopathological examinations were done, and the indium concentration in organs and serum was determined. Findings—The number of neutrophils in BALF remarkably increased in a dose-effect manner 1 and 7 days after administration and InP particles were phagocytized in the macrophages. Total protein (TP), lactate dehydrogenase (LDH), total phospholipid (TPL) and total cholesterol (T-Cho) in BALF showed a clear dose-effect relationship 7 days after administration. Indium was detected in the liver and spleen and increased in a dose-related manner on the next day and 7 days after administration. Serum indium was detected in the group given more than 10 mg/kg but did not reveal a dose relationship. Histopathological examination of the lungs showed phagocytized InP particles in the macrophages and the migration of neutrophiles in the alveoli. InP particles remained in the bronchioles and alveoli until 7 days after. No histopathological changes were detected in the liver or spleen . A hematological study did not reveal significant findings. Interpretation—Intratracheally administered InP particles cause pulmonary inflammation and those particles remain in the lower airways for at least 7 days. Phagocytosis of macrophages may contribute to their disposal and distribution to the liver and spleen. Further study is required with particles with a lower toxic activity than InP and with the same particle size as the InP used in this study, to clarify their specific toxicity. Simultaneously longer observation is needed to assess toxicity in the other organs after distribution.

Date of correction: April 07, 2006 Reason for correction: - Correction: CITATION Details: Wrong : 1) Beliles RP. Indium. In: Clayton GD, Clayton FE, eds. Patty''s industrial hygiene and toxicology. 4th ed. New York: John Wiley and Sons, 1994: 2032-2038.
2) McCord CP, Meek SF, Harrold GC, et al. The physiologic properties of indium and its compounds. J Ind Hyg Toxicol 1942; 24: 243-254.
3) Kabe I, Omae K, Nakashima H, et al. In vitro solubility and in vivo toxicity of indium phosphide. J Occup Health 1996; 38: 6-12.
4) Zheng W, Steven M, Margaret J, et al. Tissue distribution and elimination of indium in male Fischer 344 rats following oral and intratracheal administration of indium phosphide. J Toxicol Environ Health 1994; 43: 483-494.
5) Hosoda K, Omae K, Takebayashi T, et al. Determination of δ-aminolevulinic acid in blood using stopped-flow HPLC. Bunseki Kagaku 1994; 43: 311-316 (in Japanese).
6) Hosoda K, Omae K, Nakashima H, et al. Determination of indium in organs of rats using GFAAS. Jpn J Hyg 1994; 49: 216 (in Japanese).
7) Adamson RH, Canellos GP, Sieber SM. Studies on the antitumor activity of gallium nitrate (NSC-15200) and other group IIIa metal salts. Cancer Chemotherapy Reports Part 1 1975; 59: 599-610.
8) Blazka ME, Dixon D, Haskins E, et al. Pulmonary toxicity to intratracheally administered indium trichloride in Fischer 344 rats. Fundamental and Applied Toxicol 1994; 22: 231-239.
9) Downs WL, Scott JK, Steadman LT, et al. The toxicity of indium. In: Atomic energy project report No.UR-558. New York: University of Rochester, 1959: 1-57.
10) Tanaka A, Hisanaga A, Hirata M, et al. Chronic toxicity of indium arsenide and indium phosphide to the lungs of hamsters. Fukuoka Acta Medica 1996; 87: 108-115.
11) Driscoll KE, Lindenschmidt RC, Maurer JK, et al. Pulmonary response to silica or titanium dioxide: Inflammatory cells, alveolar macrophage-derived cytokines, and histopathology. Am J Respir Cell Mol Biol 1990; 2: 381-390.
12) Smith GA, Thomas RG, Scott JK. The metabolism of indium after administration of single dose to rats by intratracheal, subcutaneous, intramuscular and oral injection. Health Physics Pergamon Press 1960; 4: 101-108.

Right : 1) Beliles RP. Indium. In: Clayton GD, Clayton FE, eds. Patty's industrial hygiene and toxicology. 4th ed. New York: John Wiley and Sons, 1994: 2032-2038.
2) McCord CP, Meek SF, Harrold GC, et al. The physiologic properties of indium and its compounds. J Ind Hyg Toxicol 1942; 24: 243-254.
3) Kabe I, Omae K, Nakashima H, et al. In vitro solubility and in vivo toxicity of indium phosphide. J Occup Health 1996; 38: 6-12.
4) Zheng W, Steven M, Margaret J, et al. Tissue distribution and elimination of indium in male Fischer 344 rats following oral and intratracheal administration of indium phosphide. J Toxicol Environ Health 1994; 43: 483-494.
5) Hosoda K, Omae K, Takebayashi T, et al. Determination of δ-aminolevulinic acid in blood using stopped-flow HPLC. Bunseki Kagaku 1994; 43: 311-316 (in Japanese).
6) Hosoda K, Omae K, Nakashima H, et al. Determination of indium in organs of rats using GFAAS. Jpn J Hyg 1994; 49: 216 (in Japanese).
7) Adamson RH, Canellos GP, Sieber SM. Studies on the antitumor activity of gallium nitrate (NSC-15200) and other group IIIa metal salts. Cancer Chemotherapy Reports Part 1 1975; 59: 599-610.
8) Blazka ME, Dixon D, Haskins E, et al. Pulmonary toxicity to intratracheally administered indium trichloride in Fischer 344 rats. Fundamental and Applied Toxicol 1994; 22: 231-239.
9) Downs WL, Scott JK, Steadman LT, et al. The toxicity of indium. In: Atomic energy project report No.UR-558. New York: University of Rochester, 1959: 1-57.
10) Tanaka A, Hisanaga A, Hirata M, et al. Chronic toxicity of indium arsenide and indium phosphide to the lungs of hamsters. Fukuoka Acta Medica 1996; 87: 108-115.
11) Driscoll KE, Lindenschmidt RC, Maurer JK, et al. Pulmonary response to silica or titanium dioxide: Inflammatory cells, alveolar macrophage-derived cytokines, and histopathology. Am J Respir Cell Mol Biol 1990; 2: 381-390.
12) Smith GA, Thomas RG, Scott JK. The metabolism of indium after administration of single dose to rats by intratracheal, subcutaneous, intramuscular and oral injection. Health Physics Pergamon Press 1960; 4: 101-108.

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Abstract

Effects of Intratracheally Administered Indium Phosphide on Male Fischer 344 Rats: Takamoto UEMURA, et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University—Objective—To examine the effects of intratracheally administered indium phosphide (InP) and distribution of indium on male Fischer 344 rats. Materials and methods—Rats were intratracheally given 0, 1, 10 or 100 mg/kg of InP with a mean diameter of 0.8μm and observed for 1 and 7 days. The bronchoalveolar lavage fluid (BALF) was examined biochemically and cytologically. Serum biochemical, hematological and histopathological examinations were done, and the indium concentration in organs and serum was determined. Findings—The number of neutrophils in BALF remarkably increased in a dose-effect manner 1 and 7 days after administration and InP particles were phagocytized in the macrophages. Total protein (TP), lactate dehydrogenase (LDH), total phospholipid (TPL) and total cholesterol (T-Cho) in BALF showed a clear dose-effect relationship 7 days after administration. Indium was detected in the liver and spleen and increased in a dose-related manner on the next day and 7 days after administration. Serum indium was detected in the group given more than 10 mg/kg but did not reveal a dose relationship. Histopathological examination of the lungs showed phagocytized InP particles in the macrophages and the migration of neutrophiles in the alveoli. InP particles remained in the bronchioles and alveoli until 7 days after. No histopathological changes were detected in the liver or spleen . A hematological study did not reveal significant findings. Interpretation—Intratracheally administered InP particles cause pulmonary inflammation and those particles remain in the lower airways for at least 7 days. Phagocytosis of macrophages may contribute to their disposal and distribution to the liver and spleen. Further study is required with particles with a lower toxic activity than InP and with the same particle size as the InP used in this study, to clarify their specific toxicity. Simultaneously longer observation is needed to assess toxicity in the other organs after distribution.

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