Immunotoxic response of oleic acid anilide and its hydrolysis products in female MRL+/+ mice

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Abstract

An epidemic of a multi-systemic disease, known as the toxic oil syndrome (TOS), was caused by consumption of edible oil denatured with 2% aniline. Oleic acid anilide (OAA) has been suggested as one of the most likely etiologic agents responsible for TOS based upon its presence in high quantities in TOS-related oil samples. The aim of this study was to evaluate the immune response of OAA and contribution of its hydrolysis products (aniline and oleic acid) in the immunotoxic response. Female MRL+/+ mice were treated with equimolar doses of OAA, aniline or oleic acid (0.8 mmol/kg), i.p., twice a week for 6 weeks. The levels of immunoglobulins IgE, IgG and its isotypes (IgG1, IgG2a, IgG2b, and IgG3), and the appearance of antinuclear antibodies (ANA) were determined in the serum. Exposure to OAA and oleic acid caused significant increases in IgG, IgG1, IgG 2a, and IgG2b levels as compared to aniline and control groups, whereas IgG3 value increased only in OAA-treated mice. The IgE levels in OAA-, aniline-, and oleic acid-treated groups were higher than the controls. Among the various treatment groups, sera from 50% of the OAA-treated mice gave rise to intense homogenous fluorescence patterns on Hep-2 cells, suggesting the presence of significant levels of antinuclear antibodies (ANA). Furthermore, analysis of serum cytokines showed significant increases in G-CSF levels in OAA- and aniline-treated mice. Among the tissues examined, morphological changes were confined to the spleen, which showed increased lymphocyte population in OAA- and aniline-treated mice. These studies indicate that OAA and its hydrolysis products cause perturbations in the immune response, and could contribute to TOS-related immune derangements.

Original languageEnglish (US)
Pages (from-to)231-236
Number of pages6
JournalJournal of Immunotoxicology
Volume2
Issue number4
DOIs
StatePublished - Oct 2005

Fingerprint

Hydrolysis
Immunoglobulin G
Oils
Poisons
Oleic Acid
Antinuclear Antibodies
Immunoglobulin E
Serum
oleoylanilide
Lymphocytes
Granulocyte Colony-Stimulating Factor
aniline
Oils and fats
Immunoglobulins
Spleen
Fluorescence
Tissue
Cytokines
Control Groups
Population

Keywords

  • Aniline
  • Immunotoxicity
  • Oleic acid
  • Oleic acid anilide
  • Toxic oil syndrome

ASJC Scopus subject areas

  • Toxicology
  • Immunology
  • Immunology and Allergy

Cite this

@article{84131369a3e54f80bf54b6449afc39e4,
title = "Immunotoxic response of oleic acid anilide and its hydrolysis products in female MRL+/+ mice",
abstract = "An epidemic of a multi-systemic disease, known as the toxic oil syndrome (TOS), was caused by consumption of edible oil denatured with 2{\%} aniline. Oleic acid anilide (OAA) has been suggested as one of the most likely etiologic agents responsible for TOS based upon its presence in high quantities in TOS-related oil samples. The aim of this study was to evaluate the immune response of OAA and contribution of its hydrolysis products (aniline and oleic acid) in the immunotoxic response. Female MRL+/+ mice were treated with equimolar doses of OAA, aniline or oleic acid (0.8 mmol/kg), i.p., twice a week for 6 weeks. The levels of immunoglobulins IgE, IgG and its isotypes (IgG1, IgG2a, IgG2b, and IgG3), and the appearance of antinuclear antibodies (ANA) were determined in the serum. Exposure to OAA and oleic acid caused significant increases in IgG, IgG1, IgG 2a, and IgG2b levels as compared to aniline and control groups, whereas IgG3 value increased only in OAA-treated mice. The IgE levels in OAA-, aniline-, and oleic acid-treated groups were higher than the controls. Among the various treatment groups, sera from 50{\%} of the OAA-treated mice gave rise to intense homogenous fluorescence patterns on Hep-2 cells, suggesting the presence of significant levels of antinuclear antibodies (ANA). Furthermore, analysis of serum cytokines showed significant increases in G-CSF levels in OAA- and aniline-treated mice. Among the tissues examined, morphological changes were confined to the spleen, which showed increased lymphocyte population in OAA- and aniline-treated mice. These studies indicate that OAA and its hydrolysis products cause perturbations in the immune response, and could contribute to TOS-related immune derangements.",
keywords = "Aniline, Immunotoxicity, Oleic acid, Oleic acid anilide, Toxic oil syndrome",
author = "Ping Cai and M Khan and Bhupendra Kaphalia and Ghulam Ansari",
year = "2005",
month = "10",
doi = "10.1080/15476910500362960",
language = "English (US)",
volume = "2",
pages = "231--236",
journal = "Neurodegenerative Diseases",
issn = "1660-2854",
publisher = "S. Karger AG",
number = "4",

}

TY - JOUR

T1 - Immunotoxic response of oleic acid anilide and its hydrolysis products in female MRL+/+ mice

AU - Cai, Ping

AU - Khan, M

AU - Kaphalia, Bhupendra

AU - Ansari, Ghulam

PY - 2005/10

Y1 - 2005/10

N2 - An epidemic of a multi-systemic disease, known as the toxic oil syndrome (TOS), was caused by consumption of edible oil denatured with 2% aniline. Oleic acid anilide (OAA) has been suggested as one of the most likely etiologic agents responsible for TOS based upon its presence in high quantities in TOS-related oil samples. The aim of this study was to evaluate the immune response of OAA and contribution of its hydrolysis products (aniline and oleic acid) in the immunotoxic response. Female MRL+/+ mice were treated with equimolar doses of OAA, aniline or oleic acid (0.8 mmol/kg), i.p., twice a week for 6 weeks. The levels of immunoglobulins IgE, IgG and its isotypes (IgG1, IgG2a, IgG2b, and IgG3), and the appearance of antinuclear antibodies (ANA) were determined in the serum. Exposure to OAA and oleic acid caused significant increases in IgG, IgG1, IgG 2a, and IgG2b levels as compared to aniline and control groups, whereas IgG3 value increased only in OAA-treated mice. The IgE levels in OAA-, aniline-, and oleic acid-treated groups were higher than the controls. Among the various treatment groups, sera from 50% of the OAA-treated mice gave rise to intense homogenous fluorescence patterns on Hep-2 cells, suggesting the presence of significant levels of antinuclear antibodies (ANA). Furthermore, analysis of serum cytokines showed significant increases in G-CSF levels in OAA- and aniline-treated mice. Among the tissues examined, morphological changes were confined to the spleen, which showed increased lymphocyte population in OAA- and aniline-treated mice. These studies indicate that OAA and its hydrolysis products cause perturbations in the immune response, and could contribute to TOS-related immune derangements.

AB - An epidemic of a multi-systemic disease, known as the toxic oil syndrome (TOS), was caused by consumption of edible oil denatured with 2% aniline. Oleic acid anilide (OAA) has been suggested as one of the most likely etiologic agents responsible for TOS based upon its presence in high quantities in TOS-related oil samples. The aim of this study was to evaluate the immune response of OAA and contribution of its hydrolysis products (aniline and oleic acid) in the immunotoxic response. Female MRL+/+ mice were treated with equimolar doses of OAA, aniline or oleic acid (0.8 mmol/kg), i.p., twice a week for 6 weeks. The levels of immunoglobulins IgE, IgG and its isotypes (IgG1, IgG2a, IgG2b, and IgG3), and the appearance of antinuclear antibodies (ANA) were determined in the serum. Exposure to OAA and oleic acid caused significant increases in IgG, IgG1, IgG 2a, and IgG2b levels as compared to aniline and control groups, whereas IgG3 value increased only in OAA-treated mice. The IgE levels in OAA-, aniline-, and oleic acid-treated groups were higher than the controls. Among the various treatment groups, sera from 50% of the OAA-treated mice gave rise to intense homogenous fluorescence patterns on Hep-2 cells, suggesting the presence of significant levels of antinuclear antibodies (ANA). Furthermore, analysis of serum cytokines showed significant increases in G-CSF levels in OAA- and aniline-treated mice. Among the tissues examined, morphological changes were confined to the spleen, which showed increased lymphocyte population in OAA- and aniline-treated mice. These studies indicate that OAA and its hydrolysis products cause perturbations in the immune response, and could contribute to TOS-related immune derangements.

KW - Aniline

KW - Immunotoxicity

KW - Oleic acid

KW - Oleic acid anilide

KW - Toxic oil syndrome

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U2 - 10.1080/15476910500362960

DO - 10.1080/15476910500362960

M3 - Article

C2 - 18958679

AN - SCOPUS:29044432809

VL - 2

SP - 231

EP - 236

JO - Neurodegenerative Diseases

JF - Neurodegenerative Diseases

SN - 1660-2854

IS - 4

ER -