Benzyl isothiocyanate inhibits oxidative stress in mouse skin: Involvement of attenuation of leukocyte infiltration

Yoshimasa Nakamura; Noriyuki Miyoshi; Satoko Takabayashi; Toshihiko Osawa

doi:10.1002/biof.552210149

Benzyl isothiocyanate inhibits oxidative stress in mouse skin: Involvement of attenuation of leukocyte infiltration

Yoshimasa Nakamura, Noriyuki Miyoshi, Satoko Takabayashi, Toshihiko Osawa

Research output: Contribution to journal › Article › peer-review

15 Citations (Scopus)

Abstract

The exposure of benzyl isothiocyanate (BITC) to mouse skin resulted in the attenuation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage through not only inhibition of the NADPH oxidase system but also leukocyte clearance at inflamed region. In spite of little ability to affect TPA-induced edema formation, pretreatments of mouse skin with BITC before the first or second TPA treatment significantly decrease the H_2O_2 level. A histological study also demonstrated that BITC enhanced the terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL)-positive index in mouse skin, suggesting that BITC might accelerate the disappearance of infiltrated leukocytes. Thus, these gathered data further supported that BITC has a potential as an anti-inflammatory agent.

Original language	English
Pages (from-to)	255-257
Number of pages	3
Journal	BioFactors
Volume	21
Issue number	1-4
DOIs	https://doi.org/10.1002/biof.552210149
Publication status	Published - Jan 1 2004
Externally published	Yes

Keywords

Benzyl isothiocyanate
NADPH oxidase
Neutrophil
Reactive oxygen species
Tumor promotion

ASJC Scopus subject areas

Biochemistry
Molecular Medicine
Clinical Biochemistry

Access to Document

10.1002/biof.552210149

Cite this

@article{16622077592b414fb91074b6229eb7b9,

title = "Benzyl isothiocyanate inhibits oxidative stress in mouse skin: Involvement of attenuation of leukocyte infiltration",

abstract = "The exposure of benzyl isothiocyanate (BITC) to mouse skin resulted in the attenuation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage through not only inhibition of the NADPH oxidase system but also leukocyte clearance at inflamed region. In spite of little ability to affect TPA-induced edema formation, pretreatments of mouse skin with BITC before the first or second TPA treatment significantly decrease the H_2O_2 level. A histological study also demonstrated that BITC enhanced the terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL)-positive index in mouse skin, suggesting that BITC might accelerate the disappearance of infiltrated leukocytes. Thus, these gathered data further supported that BITC has a potential as an anti-inflammatory agent.",

keywords = "Benzyl isothiocyanate, NADPH oxidase, Neutrophil, Reactive oxygen species, Tumor promotion",

author = "Yoshimasa Nakamura and Noriyuki Miyoshi and Satoko Takabayashi and Toshihiko Osawa",

year = "2004",

month = jan,

day = "1",

doi = "10.1002/biof.552210149",

language = "English",

volume = "21",

pages = "255--257",

journal = "BioFactors",

issn = "0951-6433",

publisher = "Wiley-Blackwell",

number = "1-4",

}

TY - JOUR

T1 - Benzyl isothiocyanate inhibits oxidative stress in mouse skin

T2 - Involvement of attenuation of leukocyte infiltration

AU - Nakamura, Yoshimasa

AU - Miyoshi, Noriyuki

AU - Takabayashi, Satoko

AU - Osawa, Toshihiko

PY - 2004/1/1

Y1 - 2004/1/1

N2 - The exposure of benzyl isothiocyanate (BITC) to mouse skin resulted in the attenuation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage through not only inhibition of the NADPH oxidase system but also leukocyte clearance at inflamed region. In spite of little ability to affect TPA-induced edema formation, pretreatments of mouse skin with BITC before the first or second TPA treatment significantly decrease the H_2O_2 level. A histological study also demonstrated that BITC enhanced the terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL)-positive index in mouse skin, suggesting that BITC might accelerate the disappearance of infiltrated leukocytes. Thus, these gathered data further supported that BITC has a potential as an anti-inflammatory agent.

AB - The exposure of benzyl isothiocyanate (BITC) to mouse skin resulted in the attenuation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage through not only inhibition of the NADPH oxidase system but also leukocyte clearance at inflamed region. In spite of little ability to affect TPA-induced edema formation, pretreatments of mouse skin with BITC before the first or second TPA treatment significantly decrease the H_2O_2 level. A histological study also demonstrated that BITC enhanced the terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL)-positive index in mouse skin, suggesting that BITC might accelerate the disappearance of infiltrated leukocytes. Thus, these gathered data further supported that BITC has a potential as an anti-inflammatory agent.

KW - Benzyl isothiocyanate

KW - NADPH oxidase

KW - Neutrophil

KW - Reactive oxygen species

KW - Tumor promotion

UR - http://www.scopus.com/inward/record.url?scp=16444376996&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=16444376996&partnerID=8YFLogxK

U2 - 10.1002/biof.552210149

DO - 10.1002/biof.552210149

M3 - Article

C2 - 15630206

AN - SCOPUS:16444376996

SN - 0951-6433

VL - 21

SP - 255

EP - 257

JO - BioFactors

JF - BioFactors

IS - 1-4

ER -

Benzyl isothiocyanate inhibits oxidative stress in mouse skin: Involvement of attenuation of leukocyte infiltration

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this