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Hair Coloring
Published in Dale H. Johnson, Hair and Hair Care, 2018
The chemistry of this system has received considerable study both from the viewpoint of the types of colors that can be achieved and from the complex reaction mechanisms that are occurring. Consequently, there has been a great advance in the understanding and control of oxidative dye chemistry in the last 20 years. A number of review articles have been written describing the chemistry (14–17). In general, as shown below, the primary intermediate is oxidized to a reactive imine [10] (p-benzoquinone mono or diimine, Z=0 or NH) which then attacks electrophilic sites on the color coupler to give a diphenylamine derivative [11]. The diphenylamine is then oxidized to the indo dye [12], which is the basic chromophoric unit of the oxidation dye system. In general, blue indo dyes are formed from mixtures of p-diamines and m-diamines (X=NH2, Y=NH) or phenols, reds from p-diamines or p-aminophenols and m-aminophenols (X=NH2, Y=0), and yellow/browns from p-diamines and p-aminophenols and resorcinols (X=OH, Y=0). Thus, a full range of shades can be formulated with these relatively simple mixtures.
Cosmetic Components Causing Contact Urticaria Syndrome: An Update
Published in Ana M. Giménez-Arnau, Howard I. Maibach, Contact Urticaria Syndrome, 2014
Among the causal hair dye ingredients, the following dyes have been reported as inducers of CoU, sometimes with systemic symptoms: the permanent oxidation hair dyes para-phenylenediamine and its derivatives, such as para-aminophenol and para-methylaminophenol,[11] and para-toluenediamine.[12] The reaction seems to occur only after oxidation by H2O2 and is partially reversed when the antioxidant sodium sulfite is added to the mix. [12] Goldbert et al. were able to identify the oxidation product of para-phenylenediamine that is causing the reaction: N’N’-bis-(4-aminophenyl)-2,5-diamino-1,4-quinone-diimine.[13]
Radiopharmaceuticals for SPECT
Published in Martin G. Pomper, Juri G. Gelovani, Benjamin Tsui, Kathleen Gabrielson, Richard Wahl, S. Sam Gambhir, Jeff Bulte, Raymond Gibson, William C. Eckelman, Molecular Imaging in Oncology, 2008
Copper(II)bis(thiosemicarbazone) complexes possess redox potentials in a range where they can be reduced by intracellular components. Radiolabeled 60/62/64Cu PTSM (Fig. 8) is a nonspecific selective blood-perfusion PET Tracer (Mathias, 1990) whereas 60/62/64Cu ATSM is a PET tracer for hypoxia imaging (135). The differing biological properties of these very similar complexes (ASTM has an additional methyl group on the diimine backbone) has been explained as follows: Cu(II)PTSM, with a reduction potential of −0.53 V, diffuses into all cells where it is reduced to Cu(I)PTSM, which then dissociates and the free copper binds to cellular components. Cu(II)ATSM with a lower reduction potential of −0.59 V is also reduced in all cells but in the presence of oxygen is rapidly reoxidized where it can now diffuse out of the cell. In hypoxic cells, the lack of oxygen decreases reoxidation and permits complex dissociation with subsequent intracellular trapping of copper. Structure-activity studies (136) have shown that electron-donating substituents on both carbons of the diimine backbone are required to decrease the reduction potential (Fig. 8). All copper complexes, with this substitution pattern, showed uptake in hypoxic cells in vitro but at different rates. The uptake of Cu(II)DTS and Cu(II)DTSM were actually higher than Cu(II)ASTM at 5 to 20 minutes where as Cu(II)ASTM was highest at 1 hour (136). Cu(II)ASTM has recently been shown to be selective for certain types of hypoxic tumors (137). A limited clinical study of 60Cu (II)ASTM in cervical cancer demonstrated that tumor to muscle ratios of greater than 3.5 were predictive of disease recurrence (138).
Anti-biofilm studies of synthetic imidazolium salts on dental biofilm in vitro
Published in Journal of Oral Microbiology, 2022
Ting Pan, Feng-Shou Liu, Huancai Lin, Yan Zhou
Under nitrogen atmosphere, a mixture of α-diimine compound (1.00 mmol) and chloromethyl ethyl ether (4 mL) was stirred at 100°C overnight. Then, the solution was cooled to room temperature, treated with Et2O and stirred for another 1 h, resulting the formation of yellowish precipitate. The solid was isolated by filtration and washed with anhydrous Et2O three times. The desired imidazolium salt of C5 was obtained in 82% yield. 1H NMR (400 MHz, CDCl3) δ 11.21 (br, 1 H), 8.04 (d, J = 8.2 Hz, 2H), 7.61 (t, J = 7.6 Hz, 2H), 7.31 (d, J = 7.9 Hz, 2 H), 6.94 (s, 4 H), 3.96 (s, 6 H), 2.71–2.63 (m, 4 H), 1.35 (d, J = 6.5 Hz, 12 H), 1.16 (d, J = 6.5 Hz, 12 H). 13C NMR (101 MHz, CDCl3) δ 161.9 146.5, 137.7, 134.4, 130.5, 130.4, 129.9, 128.2, 123.1, 122.81, 121.8, 110.2, 55.5, 29.5, 24.6, 23.4.
Comparison between patch test results of natural dyes and standard allergens in batik workers with occupational contact dermatitis
Published in Cutaneous and Ocular Toxicology, 2022
Eka Devinta Novi Diana, Suci Widhiati, Moerbono Mochtar, Muhammad Eko Irawanto
Some standard allergen properties are thought to cause ACD, including having a small molecular weight (less than 500 Da), being electrophilic, and being a strong sensitiser. The study of Handa et al. in India reported that a positive patch test for PPD of 0.1% was found in 13% of cases18. In this study, out of 5 subjects with ACD due to exposure to standard allergens, a positive patch test for 0.1% PPD was found in 1 subject (20%). P-phenylenediamine is a hapten with a small molecular weight of 108.1 Da. The low molecular weight of PPD facilitates the penetration of allergens into the stratum corneum, which in turn causes sensitisation. P-phenylenediamine easily binds to proteins to form a complete antigen and is electrophilic. P-phenylenediamine sensitisation of the skin is thought to be due to the formation of benzoquinone. P-phenylenediamine, which is exposed to oxygen (O2) in the air for a long time, will be oxidised to reactive benzoquinone diimine, a necessary substance to react with proteins19.
Brief overview of antibody–drug conjugate therapy for acute leukemia
Published in Expert Opinion on Biological Therapy, 2021
Despite increasing focus on alternative forms of antigen-specific immunotherapy including bispecific antibodies and chimeric antigen receptor (CAR)-modified immune effector cells, there remains interest in using ADCs for acute leukemia, with several investigational agents currently undergoing clinical testing. One such ADC is IMGN632, which contains a cysteine-engineered humanized CD123 IgG1 antibody (G4723A) linked to a DNA mono-alkylating indolinobenzodiazepine pseudodimer (IGN) [45,46]. Compared to the same antibody conjugated to a diimine (cross-linking) containing IGN payload, this monoimine payload maintained potent anti-leukemia properties in vitro (many fold more potent than GO in many primary AML samples) but exerted substantially less toxicity toward normal myeloid progenitor cells [45]. Whether this characteristic of the payload will lead to a broadening of the therapeutic window in the clinic, as is hoped, is an open question but it is one example of a strategy pursued to reduce on-target, off-leukemia cell toxicities. IMGN632 is currently tested in a phase 1 trial in patients with relapsed/refractory AML, BPDCN, ALL and other CD123-expressing hematological malignancies (NCT03386513) [47] as well as in a phase 1b/2 trial as monotherapy or with venetoclax and/or azacytidine in adults with CD123+ AML (NCT04086264) [48]. Clinical activity of IMGN632 in acute leukemia is indicated by interim analyses of the phase 1 trial showing achievement of a CR, CRi, or a morphologic leukemia-free state in 13 of 66 patients with relapsed/refractory AML across a wide range of drug doses [47].