Acrolein—an α,ß-Unsaturated Aldehyde: A Review of Oral Cavity Exposure and Oral Pathology Effects

Aizenbud, Dror; Aizenbud, Itay; Reznick, Abraham Z.; Avezov, Katia

doi:10.5041/rmmj.10251

Cited by 31 publications

(21 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have suggested that a high level of oral exposure to Acr through consumption of food or other sources induces detrimental effects on the oral cavity, including salivary quality and contents, oral resistance to oxidative stress, and stress mechanism activation in a variety of oral cells (Aizenbud, Aizenbud, Reznick, & Avezov, ). Here, we found that acrolein‐induced DNA adducts, that is Acr‐dG adducts, were significantly increased in buccal cells after 2‐hr and 6‐hr‐consuming fried food (Figure ) and the levels were not decreased after 24‐hr‐consuming fried food, indicating that Acr‐dG adducts were not repaired.…”

Section: Discussionmentioning

confidence: 99%

Identification of acrolein metabolites in human buccal cells, blood, and urine after consumption of commercial fried food

Wang¹,

Liu²,

Tsou³

et al. 2019

Food Science & Nutrition

View full text Add to dashboard Cite

Scope Acrolein is a highly electrophilic α,β‐unsaturated aldehyde and is associated with human diseases. It is formed by Maillard reaction during food processing and could be detected in the emissions of overheated cooking oils. Consequently, humans are at risk of acrolein exposure through consumption of such prepared food. Methods and results We conducted three human studies that healthy subjects (21–30 years) were served fried foods including fried chicken and French fries from three commercial fast food restaurants. Acrolein‐related metabolites including urinary 3‐hydroxypropyl mercapturic acid (3‐HPMA), serum acrolein‐protein conjugates (Acr‐FDP), and buccal acrolein‐induced DNA damages (Acr‐dG adducts) along with GSH levels in serum or buccal cells were investigated for different times after consumption. Conclusion Urinary 3‐HPMA levels were increased after 2‐hr consumption of fried food with an elimination half‐life of 10 hr. In addition, increased Acr‐dG adducts in oral cavity were inversely correlated to buccal glutathione (GSH) levels after consumption. However, there was no significant change in systemic GSH levels or Acr‐FDP adducts in serum. These results indicate that exposure of acrolein from consuming fried food affects local oral cavity homeostasis. This may provide a possible link between intake of fried food and increased risk of upper aerodigestive tract cancers.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of acrolein metabolites in human buccal cells, blood, and urine after consumption of commercial fried food

Wang¹,

Liu²,

Tsou³

et al. 2019

Food Science & Nutrition

View full text Add to dashboard Cite

show abstract

“…One limitation of our study is that we could not exclude other exposure possibilities to Acr other than CS. Acr is an important pollutant that is widely distributed in the environment because it is a prominent byproduct of the incomplete combustion of organic matter and is also formed from carbohydrates, vegetable oils, animal fats, and amino acids during the heating of foods (18,50). Therefore, humans are exposed to Acr by the inhalation of incompletely combusted organic matter and overheated cooking oil fumes or by the ingestion of many foods (51).…”

Section: Discussionmentioning

confidence: 99%

“…However, smoking of tobacco products is equivalent to or exceeds the total human exposure to Acr from all other sources (52). Previous studies have suggested that a high level of oral exposure to Acr through these sources induces detrimental effects on the oral cavity, including salivary quality and contents, oral resistance to oxidative stress, and stress mechanism activation in a variety of oral cells (50). Therefore, protective pathways against Acr-induced cytotoxicity in the oral cavity need to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

Tsou¹,

Hu²,

Liu³

et al. 2019

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Background: Cigarette smoking (CS) and betel quid (BQ) chewing are two known risk factors and have synergistic potential for the development of oral squamous cell carcinoma (OSCC) in Taiwan. The p53 mutation characteristics in OSCC (G to A or G to T mutations) are similar to that of acrolein-induced DNA damage. Acrolein is a major cigarette-related carcinogen that preferentially causes p53 mutations and inhibits DNA repair function in lung cancer. We hypothesize that acrolein is associated with OSCC carcinogenesis.Methods: A total of 97 patients with OSCC and 230 healthy subjects with CS and/or BQ chewing histories were recruited. Slot blot analysis of Acr-dG adducts, an indicator of acrolein-induced DNA damage in buccal DNA, and LC/MS-MS analysis of 3-HPMA levels, urinary Acr metabolites, were performed.Results: Our results showed that the level of Acr-dG adducts in buccal cells was 1.4-fold higher in patients with OSCC than in healthy subjects with CS and/or BQ chewing histories (P < 0.001). In addition, in healthy subjects, CS and BQ chewing were associated with significantly higher levels of 3-HPMA, indicating that CS and BQ chewing promotes acrolein absorption. However, 3-HPMA levels in patients with OSCC were significantly lower than those in healthy subjects, indicating impaired acrolein metabolism.Conclusions: In this study, we provide a novel mechanism by which increased acrolein uptake and impaired metabolism may contribute to the synergistic potential of CS and BQinduced OSCC.Impact: Elevated acrolein-induced DNA damage (Acr-dG adducts) detected in buccal swabs may serve as an early indicator to identify patients at risk of developing OSCC. a The P < 0.05 versus smoking (CS) by Student t test.

show abstract

“…Acrolein is the most reactive 2-alkenal commonly detected in pollution, burning of fat-containing foods, and smoking. It is thus mainly considered to be an environmental pollutant, exposure to which by inhalation induces severe irritating effects on mucous membranes, especially in the eyes and upper respiratory tract [22]. However, acrolein can also be produced endogenously by lipid peroxidation.…”

Section: Acroleinmentioning

confidence: 99%

Lipid Oxidation Products in the Pathogenesis of Inflammation-related Gut Diseases

Sottero

Rossin

Poli

et al. 2018

CMC

View full text Add to dashboard Cite

In this review we summarize the current knowledge on the role of lipid oxidation products in regulating redox pathways involved in the pathogenesis of inflammation- related gut diseases. In particular, lipid peroxidation end products, such as isoprostanes and aldehydes, and cholesterol oxidation-derived oxysterols are taken into consideration. The control of oxidative damage and consequently tissue local over-production of lipid oxidation products by using specific antioxidant and anti-inflammatory molecules in the diet may have clinical and therapeutic benefits.

show abstract

Acrolein—an α,ß-Unsaturated Aldehyde: A Review of Oral Cavity Exposure and Oral Pathology Effects

Cited by 31 publications

References 62 publications

Identification of acrolein metabolites in human buccal cells, blood, and urine after consumption of commercial fried food

Identification of acrolein metabolites in human buccal cells, blood, and urine after consumption of commercial fried food

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

Lipid Oxidation Products in the Pathogenesis of Inflammation-related Gut Diseases

Contact Info

Product

Resources

About