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Monographs of essential oils that have caused contact allergy / allergic contact dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
In a number of publications, positive patch tests to cinnamon oil have been reported with unknown, uncertain or unstated relevance. These include (literature screened up to 2014 [27]) the following. A positive patch test to cinnamon oil was seen in a patient working in a cosmetic factory who had occupational dermatitis from 2-bromo-2-nitropropane-1,3-diol (8). Two patients with contact dermatitis reacted to both cinnamon oil and its main ingredient, cinnamal (15). Another individual showed a positive patch test reaction to cinnamon oil, possibly from its presence in a topical pharmaceutical preparation (12).
Global Regulation of Preservatives and Cosmetic Preservatives
Published in Philip A. Geis, Cosmetic Microbiology, 2020
The CIR process determined that chloroacetamide is unsafe for use in cosmetics. The following preservatives presented problems and as of this writing have insufficient data status: Benzylparaben (2019)Sodium iodate (1995—no reported uses)Glutaral2-Bromo-2-nitropropane-1,3-diol and 5-bromo-5-nitro-1,3 dioxane when used where amines and nitrosamines could be formedFormaldehyde in aerosols
Common Cosmetic Ingredients: Chemistry, Actions, Safety and Products
Published in Heather A.E. Benson, Michael S. Roberts, Vânia Rodrigues Leite-Silva, Kenneth A. Walters, Cosmetic Formulation, 2019
Bronopol (2-bromo-2-nitropropane-1,3-diol) appears to have a very low frequency of dermal irritation (Frosch et al., 1990). People who are sensitive to formaldehyde are also likely to be sensitive to bronopol. Research indicates that bronopol may cause toxicity to cells following UV irradiation indicating that it may be problematic if products containing bronopol are applied to the skin prior to sun exposure; however, this still remains to be determined (Placzek et al., 2005).
An in silico kinetic model of 8-oxo-7,8-dihydro-2-deoxyguanosine and 8-oxo-7,8-dihydroguanosine metabolism from intracellular formation to urinary excretion
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2021
Anders Jorgensen, Maria Bremholm Thygesen, Uffe Kristiansen, Henrik Enghusen Poulsen
Urinary 8-oxo-7,8-dihydro-2-deoxyguanosine (8-oxodG) is the most well-validated marker of systemic oxidative stress on DNA; a phenomenon of paramount importance in many physiological and pathophysiological processes, such as aging, cancer development and neurodegeneration. The compound is formed by the oxidatively generated modification of guanine nucleotides by reactive oxygen species (ROS). It is found in isolated DNA, plasma, urine, and other matrices and the corresponding ribonucleoside, 8-oxo-7,8-dihydroguanosine (8-oxoGuo), is likewise found in isolated RNA, plasma (unpublished), urine and other matrices [1–3]. The exact intracellular origins of 8-oxodG (and 8-oxoGuo) and the processes leading to their eventual excretion in urine have not been established, and the enzymatic repair processes initially assumed to remove the oxidized guanine moiety (e.g. base excision repair) are apparently not responsible [4]. Oxidatively generated damage to DNA by 2-nitropropane in experimental animals induces 8-oxodG in several organs, and the number of intra-DNA 8-oxodG units generated roughly corresponds to the number of 8-oxodG molecules found in urine the following 0–24 h, where the levels of intra-DNA lesions in the organs are back to baseline level [5]. In urine, both the oxidized base and nucleoside are found; the oxidized base in about five-fold higher concentrations [6]. Our group has focused on the oxidized nucleosides, because this allows differentiation between the DNA and the RNA form. We have demonstrated this to be clinically important, particularly in type-2 diabetes where the ribonucleoside, but not the 2′-deoxyribonucleoside, is prognostic for the all-cause mortality and mortality from cardiovascular disease [7]. We have also found that neuropsychiatric disorders and interventions may have different impact on the DNA vs. the RNA marker [8,9].