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Piebaldism
Published in Electra Nicolaidou, Clio Dessinioti, Andreas D. Katsambas, Hypopigmentation, 2019
Jovan Lalošević, Miloš Nikolić
Piebaldism is a disease in which depigmented skin areas are unresponsive to topical or light treatment. The nonpigmented patches are at an increased risk of sunburn and skin cancer related to excessive sun exposure; therefore, sunscreen should be used frequently. Topical treatments with makeup or artificial pigmenting agents, for example, dihydroxyacetone (the ingredient used in sunless tanning products) that causes the skin to turn brown/dark by polymerizing the amino acids and amino groups, could be used in patients who are still not old enough for grafting procedures.36
Chemical Reactions of Glycerine
Published in Eric Jungermann, Norman O.V. Sonntag, Glycerine, 2018
Oxidation of glycerine with bromine and sodium carbonate results in the formation of a mixture of glyceraldehyde and dihydroxacetone; this mixture is often called glycerose. The aldehyde is the predominant component in this mixture. These compounds are the simplest aldose and ketose, and as such are the forerunners of the carbohydrates. Dihydroxyacetone, can also be formed by the microbiological oxidation of glycerine by the sorbose bacterium which exclusively attacks secondary hydroxyl groups [41]. Dihydroxyacetone is a skin-tanning agent and is used in cosmetic formulations designed for this purpose. Anodic oxidation of glycerol at a silver oxide electrode yields glyceric acid [42]. Glycerine is also converted into glyceric acid by the reaction of concentrated nitric acid.
Phosphatidate Phosphohydrolase Activity in the Liver
Published in David N. Brindley, John R. Sabine, Phosphatidate Phosphohydrolase, 2017
Coleman and Haynes86 also demonstrated an increase in the capacity of the liver to synthesize glycerolipids just before birth and during the days immediately afterwards. The specific activities of acyl-CoA synthetase, lysophosphatidate acyltransferase, diacylglycerol cholinephosphotransferase, and diacylglycerol acyltransferase increased by 1.4- to 3.4-fold in the 4 days before birth. After birth, lysophosphatidate acyltransferase, choline phosphotransferase, and acyl-CoA synthetase increased by five- to tenfold by the eighth day post partum. The microsomal esterification of glycerol phosphate and dihydroxyacetone phosphate was undetectable until 3 days before birth and both activities increased by about 74-fold by the fifth day after birth.
Cytotoxic, genotoxic, and toxicogenomic effects of dihydroxyacetone in human primary keratinocytes
Published in Cutaneous and Ocular Toxicology, 2021
Anneliese Striz, Ana DePina, Robert Jones, Xiugong Gao, Jeffrey Yourick
Dihydroxyacetone (DHA) is a simple ketose and the common colour-inducing ingredient in sunless tanning products. The sunless tanning colour produced is due to a non-enzymatic glycation reaction in which a reducing sugar, such as DHA, reacts with amino acids in the stratum corneum of the skin. The colour formed by this reaction, known as the Maillard reaction, will eventually be sloughed off with the stratum corneum, making it necessary to reapply these products to maintain the “tan.” In 1973, the FDA approved DHA as a colour additive exempt from certification for use in externally applied drugs and cosmetics intended solely or in part to impart colour to the human body in amounts consistent with a good manufacturing practice. (Code of Federal Regulations, Title 21, Part 73, Sections 73.1150 and 73.2150, 2020). Conventional sunless tanning products contain up to 15% DHA1.
Repurposing of rabeprazole as an anti-Trypanosoma cruzi drug that targets cellular triosephosphate isomerase
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Itzhel García-Torres, Ignacio De la Mora-De la Mora, Gabriel López-Velázquez, Nallely Cabrera, Luis Antonio Flores-López, Ingeborg Becker, Juliana Herrera-López, Roberto Hernández, Ruy Pérez-Montfort, Sergio Enríquez-Flores
MGO has a significant capacity to generate AGEs in proteins, which in turn affects protein function, leading to exhaustive cellular toxicity84, therefore compromising cell integrity. We demonstrated an increase in AGEs levels of more than 50 times, compared to the condition without treatment (Figure 4). Unfortunately, to date, no studies have been reported on the production of AGEs in T. cruzi and there are even no studies on this subject with other trypanosomes. However, it was shown that omeprazole succeeds in inhibiting the activity of TIM in the intestinal parasite Giardia lamblia, which concomitantly led to a significative increase in AGE levels, by almost 12 times with respect to the condition without the drug, consequently causing the death of the parasite44. Additionally, it has been shown that the accumulation of dihydroxyacetone can become toxic in the bloodstream forms of T. brucei. It was shown that it can have an anti-proliferative effect because of the non-enzymatic glycation named Maillard reaction, which is generated when AGEs are formed. Therefore, the authors suggested that this glycation phenomenon could contribute to the death of T. brucei by autophagy85. The foregoing evidence demonstrates that this type of damage to biomolecules (e.g. generation of AGEs) in parasite proteins can induce very negative effects on viability, as we demonstrated in this study. Moreover, toxicity mediated by highly reactive metabolites has also been reported as a mechanism of action of Bzn, one of the drugs used for the treatment of CD. In this context, Bzn must be activated by a type 1 nitroreductase (NTR) that catalyses the reduction of the nitroimidazole motif to hydroxylamine, which is subsequently converted to the highly reactive metabolite dialdehyde glyoxal, capable of forming adducts with proteins, DNA/RNA and small molecules such as glutathione7. Therefore, the mechanism of action of Bzn and Rbz share some similarities, with the advantage that no severe adverse effects have been reported for Rbz.