Genotoxicity and oxidative stress of the mutagenic compounds formed in fumes of heated soybean oil, sunflower oil and lard

Dung, Cheng-Huang; Wu, She–Ching; Yen, Gow‐Chin

doi:10.1016/j.tiv.2005.08.019

Cited by 63 publications

(50 citation statements)

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“…At 300°C, the average yield of total aliphatic aldehydes is less than 0.5 mm⅐mg Ϫ1 ⅐min Ϫ1 from most types of oil (5,12). The average yield of total aldehydes from soybean and lard oil at 150°C, however, is ϳ1.5 ppm⅐mg Ϫ1 ⅐min Ϫ1 , indicating that components of lard are pyrolyzed at lower temperatures (12).…”

Section: Discussionmentioning

confidence: 99%

“…The average yield of total aldehydes from soybean and lard oil at 150°C, however, is ϳ1.5 ppm⅐mg Ϫ1 ⅐min Ϫ1 , indicating that components of lard are pyrolyzed at lower temperatures (12). Pork lard at temperatures of 350 -400°C produces the highest amount of formaldehyde (10.9 mm ⅐ mg Ϫ1 ⅐ min Ϫ1 ), acetaldehyde (1.04 ppm ⅐ mg Ϫ1 ⅐ min Ϫ1 ), and acrolein (0.66 ppm⅐mg Ϫ1 ⅐min Ϫ1 ) via thermolytic decomposition and oxygenation of saturated fatty acids (5). These hydroxyalkenal compounds of lipid peroxidation lead to decreased antioxidant enzyme activity, in particular that of glutathione (GSH; an antioxidant enzyme that mediates cellular metabolism and homeostasis against free radical damage through the GSH redox cycle; Ref.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental trials have characterized the cytotoxic and genotoxic effects of methanolic extracts of various oil fume variants (sunflower, soybean, and lard) on human lung carcinoma cells with respect to ROS/NO formation (5,10,24). However, the precise role that SP plays in mediating neurogenic inflammation through interaction with NK-1 receptor and NK-2 receptor and consequent ROS and ICAM-1 formation following oil smoke exposure (OSE) is unclear.…”

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confidence: 99%

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Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Li P-C, Chen W-C, Chang L-C, Lin S-C. Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure. Am J Physiol Lung Cell Mol Physiol 294: L912-L920, 2008. First published March 7, 2008 doi:10.1152/ajplung.00443.2007.-This study aimed to 1) assess whether substance P (SP) acts via neurokinin (NK)-1 and NK-2 receptors to stimulate neurogenic inflammation (indicated by formation of ICAM-1 expression and oxidative stress) following oil smoke exposure (OSE) in rats; and 2) determine if pretreatment with antioxidants ameliorates the deleterious effects of OSE. Rats were pretreated with NK-1 receptor antagonist CP-96345, NK-2 receptor antagonist SR-48968, vitamin C, or catechins. OSE was for 30 -120 min. Rats were killed 0 -8 h later. Total lung resistance (RL), airway smooth muscle activity (ASMA), lung ICAM-1 expression, neurogenic plasma extravasation (via India ink and Evans blue dye), bronchoalveolar lavage fluid SP concentrations, and reactive oxygen species formation [via lucigenin-and luminalamplified chemiluminescence (CL)] were assessed. Lung histology was performed. SP concentrations increased significantly in nonpretreated rats following OSE in a dose-dependent manner. RL and total ASMA increased over time after OSE. Vitamin C and catechin pretreatments were associated with significantly reduced lucigenin CL 2 and 4 h after OSE. Pretreatment with catechins significantly reduced luminal CL counts 4 and 8 h after OSE. Evans blue levels were significantly reduced following 60 and 120 min of OSE in catechinand CP-96345-pretreated rats. ICAM-1 protein expression was significantly decreased in all pretreatment groups after OSE. Thickening of the alveolar capillary membrane, focal hemorrhaging, interstitial pneumonitis, and peribronchiolar inflammation were apparent in OSE lungs. These findings suggest that SP acts via the NK-1 receptor to provoke neurogenic inflammation, oxidative stress, and ICAM-1 expression after OSE in rats.reactive oxygen species; intracellular adhesion molecule-1; acute lung injury ACTIVATION OF NONMYELINATED bronchopulmonary C-fiber endings by various stimuli [including cigarette smoke (9), airway surface osmolality changes (14), and fire smoke (22)] causes the release of tachykinins and calcitonin gene-related peptide neuropeptides stored in the peripheral nerve terminals, eliciting both central nervous system (CNS) and local axon reflex responses (4). The CNS reflex consists of bronchoconstriction, expiratory apnea, rapid shallow breathing, cough, hypotension, and bradycardia, whereas the axon reflex response initiates local inflammation, increased mucous secretion, and bronchoconstriction. Substance P (SP), a tachykinin neuropeptide, induces a range of neuroimmunogenic effects on target smooth muscle or parasympathetic ganglia cells expressing neurokinin (NK)-1 or NK-2 receptors (1, 2). These effects, collectively termed neurogenic airway inflammation, comprise bronchoconstriction, microvasc...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Some of these can cause cancer [Wu et al 2001;Jansson et al 2006], especially with increasing cooking temperature BACkgRound (Continued) [Overvik et al 1990]. Fumes from heated peanut oil, soybean oil, sunflower oil, and lard have been shown to have mutagenic effects on lung cells in laboratory experiments [Wu and Yen 2004;Dung et al 2006].…”

Section: Exposures In Food Service Workersmentioning

confidence: 99%

Health hazard evaluation report: HETA-2008-0125, 0126, 0127-3093, respiratory symptoms in workers at three commercial kitchens, Aramark, New York, New York.

2009

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“…In addition, it has been shown that extracts of oil fumes from soybean oil, sunflower oil and lard cause cytotoxicity and oxidative DNA damage in human A-549 cells. These fume extracts contained not only trans,trans-2,4-decadienal but also trans-2-decenal, trans,trans-2,4-nonadienal and trans-2-undecenal (Dung et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Exposure to Mutagenic Aldehydes and Particulate Matter During Panfrying of Beefsteak with Margarine, Rapeseed Oil, Olive Oil or Soybean Oil

Sjaastad

Svendsen

2008

The Annals of Occupational Hygiene

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Objectives: The aim of the study was to see if a cook could be exposed to mutagenic aldehydes in fumes from frying of beefsteak using margarine, rapeseed oil, soybean oil or virgin olive oil as frying fat. In addition, levels of particle exposure were measured to make the results comparable to other studies. Methods: The levels of higher aldehydes and total particles were measured in the breathing zone of the cook during the panfrying of beefsteak with the four different frying fats. In addition, the number of particles in the size intervals 0.3-0.5, 0.5-0.7 and 0.7-1.0 mm in the kitchen was registered. Results: Measured levels of mutagenic aldehydes were between non-detectable and 25.33 mg m 23 air. The exposure level of total aerosol was between 1.0 and 11.6 mg m 23. Conclusions: Higher aldehydes were detected in all samples from this study, and mutagenic aldehydes were detected in most of the samples. Frying with margarine gave statistically significantly higher levels of mutagenic aldehydes and particles in all three size fractions than frying with the three different kinds of oil.

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Genotoxicity and oxidative stress of the mutagenic compounds formed in fumes of heated soybean oil, sunflower oil and lard

Cited by 63 publications

References 32 publications

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Health hazard evaluation report: HETA-2008-0125, 0126, 0127-3093, respiratory symptoms in workers at three commercial kitchens, Aramark, New York, New York.

Exposure to Mutagenic Aldehydes and Particulate Matter During Panfrying of Beefsteak with Margarine, Rapeseed Oil, Olive Oil or Soybean Oil

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