Review of the carcinogenic activity of diethanolamine and evidence of choline deficiency as a plausible mode of action

Leung, Hon‐Wing; Kamendulis, Lisa M.; Stott, William T.

doi:10.1016/j.yrtph.2005.08.001

Cited by 22 publications

(22 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The genotoxic activity of DEA has been extensively evaluated, and results have been consistently negative (8), with the noticeable exception of the genetic alteration in the Catnb gene in hepatocellular neoplasms of B6C3F1 mice after exposure to DEA for 2 years (9). Several excellent reviews exist that summarize the toxicology of DEA (8). In this study we examine, for the first time, whether DEA adversely affects brain development.…”

mentioning

confidence: 96%

“…However, long-term toxicity studies found an association between an increase of liver and kidney tumors in F344/N rats and B6C3F1 mice and the application of DEA (5-7). The genotoxic activity of DEA has been extensively evaluated, and results have been consistently negative (8), with the noticeable exception of the genetic alteration in the Catnb gene in hepatocellular neoplasms of B6C3F1 mice after exposure to DEA for 2 years (9). Several excellent reviews exist that summarize the toxicology of DEA (8).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus

Craciunescu¹,

Wu²,

Zeisel³

2006

FASEB j.

View full text Add to dashboard Cite

Diethanolamine (DEA) is present in many consumer products such as shampoo. Dermal administration of DEA diminishes hepatic stores of the essential nutrient choline, and we previously reported that dietary choline deficiency during pregnancy reduces neurogenesis and increases apoptosis in the hippocampus of fetal rats and mice. Therefore, DEA could also alter brain development. Timed-pregnant C57BL/6 mice were dosed dermally from gestation day 7 through 17 with DEA at 0, 20, 80, 160, 320, and 640 mg/kg body/day. At doses of DEA > 80 mg/kg body/day, we observed decreased litter size. In fetuses (embryonic day 17) collected from dams treated dermally with 80 mg/kg body/day DEA, we observed decreased neural progenitor cell mitosis at the ventricular surface of the ventricular zone of the hippocampus [to 56+/-14% (se) histone 3 (H3) phosphorylation as compared to controls; P < 0.01]. We also observed increased apoptosis in fetal hippocampus (to 170+/-10% of control measured using TUNEL and to 178+/-7% of control measured using activated caspase 3; P < 0.01). Thus, maternal exposure to DEA reduces the number of neural progenitor cells in hippocampus by two mechanisms, and this could permanently alter memory function in offspring of mothers exposed to this common ingredient of shampoos and soaps.

show abstract

mentioning

confidence: 96%

mentioning

confidence: 99%

Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus

Craciunescu¹,

Wu²,

Zeisel³

2006

FASEB j.

View full text Add to dashboard Cite

show abstract

“…Hypomethylation occurred in CG-rich regions that were associated with liver tumorigenesis. As choline is an essential nutrient in all mammals, these data indicate the initiation of liver cancer from DEA-induced choline deficiency found in mice may be applicable to humans (Leung et al, 2005;Bachman et al, 2006).…”

Section: Organic and Endocrine Active Compoundsmentioning

confidence: 77%

Epigenetic Manifestation of Environmental Exposures

Dolinoy¹,

Anderson²,

Rozek³

2011

Nutrition in Epigenetics

View full text Add to dashboard Cite

“…Leung et al reviewed the information available and also felt that choline deficiency is the mechanism responsible for liver tumor promotion in mice. 66 The localization of b-catenin protein in hepatocellular neoplasms and hepatoblastomas in B6C3F1 mice exposed dermally to 0 to 160 mg/kg bw diethanolamine for 2 years were characterized, and genetic alterations in the Catnb and H-ras genes were evaluated. 67 A lack of H-ras mutations in hepatocellular neoplasms and hepatoblastomas led the researchers to suggest that the signal transduction pathway is not involved in the development of liver tumors following diethanolamine administration.…”

Section: Dermalmentioning

confidence: 99%

“…Leung et al reviewed the information available and also felt that choline deficiency is the mechanism responsible for liver tumor promotion in mice. 66…”

Section: Carcinogenicitymentioning

confidence: 99%

Safety Assessment of Diethanolamine and Its Salts as Used in Cosmetics

et al. 2017

View full text Add to dashboard Cite

The Cosmetic Ingredient Review (CIR) Expert Panel assessed the safety of diethanolamine and its salts as used in cosmetics. Diethanolamine functions as a pH adjuster; the 16 salts included in this rereview reportedly function as surfactants, emulsifying agents, viscosity increasing agents, hair or skin conditioning agents, foam boosters, or antistatic agents. The Panel reviewed available animal and clinical data, as well as information from previous CIR reports. Since data were not available for each individual ingredient, and since the salts dissociate freely in water, the Panel extrapolated from previous reports to support safety. The Panel concluded that diethanolamine and its salts are safe for use when formulated to be nonirritating. These ingredients should not be used in cosmetic products in which N-nitroso compounds can be formed.

show abstract

Review of the carcinogenic activity of diethanolamine and evidence of choline deficiency as a plausible mode of action

Cited by 22 publications

References 58 publications

Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus

Diethanolamine alters neurogenesis and induces apoptosis in fetal mouse hippocampus

Epigenetic Manifestation of Environmental Exposures

Safety Assessment of Diethanolamine and Its Salts as Used in Cosmetics

Contact Info

Product

Resources

About