Hasegawa A - Search Results

1

Metabolic methylation is a possible genotoxicity-enhancing process of inorganic arsenics.

Yamanaka K, Hayashi H, Tachikawa M, Kato K, Hasegawa A, Oku N, Okada S. Yamanaka K, et al. Among authors: hasegawa a. Mutat Res. 1997 Nov 27;394(1-3):95-101. doi: 10.1016/s1383-5718(97)00130-7. Mutat Res. 1997. PMID: 9434848

2

DNA single-strand breaks in L-132 cells resulting from inhibition of repair polymerization shortly after exposure to dimethylarsinic acid.

Yamanaka K, Hayashi H, Kato K, Hasegawa A, Oku N, Okada S. Yamanaka K, et al. Among authors: hasegawa a. Biol Pharm Bull. 1997 Feb;20(2):163-7. doi: 10.1248/bpb.20.163. Biol Pharm Bull. 1997. PMID: 9057979 Free article.

3

Cell-nuclear accumulation of 72-kDa stress protein induced by dimethylated arsenics.

Kato K, Yamanaka K, Nakano M, Hasegawa A, Oku N, Okada S. Kato K, et al. Among authors: hasegawa a. Biol Pharm Bull. 1997 Apr;20(4):364-9. doi: 10.1248/bpb.20.364. Biol Pharm Bull. 1997. PMID: 9145211 Free article.

4

Dimethylarsinic acid exposure causes accumulation of Hsp72 in cell nuclei and suppresses apoptosis in human alveolar cultured (L-132) cells.

Kato K, Yamanaka K, Hasegawa A, Okada S. Kato K, et al. Among authors: hasegawa a. Biol Pharm Bull. 1999 Nov;22(11):1185-8. doi: 10.1248/bpb.22.1185. Biol Pharm Bull. 1999. PMID: 10598025 Free article.

5

72-kDa stress protein (hsp72) induced by administration of dimethylarsinic acid to mice accumulates in alveolar flat cells of lung, a target organ for arsenic carcinogenesis.

Kato K, Yamanaka K, Nakano M, Hasegawa A, Okada S. Kato K, et al. Among authors: hasegawa a. Biol Pharm Bull. 2000 Oct;23(10):1212-5. doi: 10.1248/bpb.23.1212. Biol Pharm Bull. 2000. PMID: 11041253 Free article.

6

Oral exposure of dimethylarsinic acid, a main metabolite of inorganic arsenics, in mice leads to an increase in 8-Oxo-2'-deoxyguanosine level, specifically in the target organs for arsenic carcinogenesis.

Yamanaka K, Takabayashi F, Mizoi M, An Y, Hasegawa A, Okada S. Yamanaka K, et al. Among authors: hasegawa a. Biochem Biophys Res Commun. 2001 Sep 14;287(1):66-70. doi: 10.1006/bbrc.2001.5551. Biochem Biophys Res Commun. 2001. PMID: 11549254

7

Preferential increase of heterochromatin in venular endothelium of lung in mice after administration of dimethylarsinic acid, a major metabolite of inorganic arsenics.

Nakano M, Yamanaka K, Hasegawa A, Sawamura R, Okada S. Nakano M, et al. Among authors: hasegawa a. Carcinogenesis. 1992 Mar;13(3):391-3. doi: 10.1093/carcin/13.3.391. Carcinogenesis. 1992. PMID: 1547528

8

Cellular response to oxidative damage in lung induced by the administration of dimethylarsinic acid, a major metabolite of inorganic arsenics, in mice.

Yamanaka K, Hasegawa A, Sawamura R, Okada S. Yamanaka K, et al. Among authors: hasegawa a. Toxicol Appl Pharmacol. 1991 Apr;108(2):205-13. doi: 10.1016/0041-008x(91)90111-q. Toxicol Appl Pharmacol. 1991. PMID: 2017750

9

Induction of DNA damage by dimethylarsine, a metabolite of inorganic arsenics, is for the major part likely due to its peroxyl radical.

Yamanaka K, Hoshino M, Okamoto M, Sawamura R, Hasegawa A, Okada S. Yamanaka K, et al. Among authors: hasegawa a. Biochem Biophys Res Commun. 1990 Apr 16;168(1):58-64. doi: 10.1016/0006-291x(90)91674-h. Biochem Biophys Res Commun. 1990. PMID: 2158319

10

DNA damage induced in cultured human alveolar (L-132) cells by exposure to dimethylarsinic acid.

Kato K, Hayashi H, Hasegawa A, Yamanaka K, Okada S. Kato K, et al. Among authors: hasegawa a. Environ Health Perspect. 1994 Sep;102 Suppl 3(Suppl 3):285-8. doi: 10.1289/ehp.94102s3285. Environ Health Perspect. 1994. PMID: 7843116 Free PMC article.

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