Semiquinone Anion Radicals of Catechol(amine)s, Catechol Estrogens, and Their Metal Ion Complexes

Kalyanaraman, B.; Felix, C. C.; Sealy, R. C.

doi:10.2307/3430009

Cited by 28 publications

(32 citation statements)

References 64 publications

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“…For instance, the g iso value for the deprotonated (anionic) radical derived from catechol amounted to 2.0046 (Kalyanaraman et al, 1985); the g x , g y and g z values determined for the deprotonated semiquinone derivative of 3,4-dihydroxybenzoic acid amounted to 2.0062, 20057 and 2.0026, respectively (Witwicki et al, 2009b); for monoprotonated benzosemiquinone the values were 2.0066, 20051 and 2.0022, respectively (Flores et al, 2012); and for the transient radicals of humic acids they were 2.0055, 2.0055 and 2.0023, respectively (Christoforidis et al, 2007). The low values of g x , g y and g z observed for the radical systems obtained in the reaction with Hg(II) strongly suggest the formation of Hg(II)-semiquinone complexes.…”

Section: Hg(ii) Radical Complexes Derived From Model Compoundsmentioning

confidence: 99%

Understanding natural semiquinone radicals – Multifrequency EPR and relativistic DFT studies of the structure of Hg(II) complexes

2015

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Multifrequency EPR spectroscopy and DFT calculations were used to investigate Hg(II) complexes with semiquinone radical ligands formed in a direct reaction between the metal ions and tannic acid (a polyphenol closely related to tannins). Because of the intricate structure of tannic acid a vast array of substituted phenolic compounds were tested to find a structural model mimicking its ability to react with Hg(II) ions. The components of the g matrix (the g tensor) determined from the high field (208 GHz) EPR spectra of the Hg(II) complexes with the radical ligands derived from tannic acid and from the model compounds were analogous, indicating a similar coordination mode in all the studied Hg(II) complexes. Since catechol (1,2-dihydroxybenzene) was the simplest compound undergoing the reaction with Hg(II) it was selected for DFT studies which were aimed at providing an insight into the structural properties of the investigated complexes. Various coordination numbers and different conformations and protonation states of the ligands were included in the theoretical analyses. g Matrices were computed for all the DFT optimized geometries. A good agreement between the theoretical and experimental values was observed only for the model with the Hg(II) ion tetracoordinated by two ligands, one of the ligands being monoprotonated with the unpaired electron mainly localized on it.

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Section: Hg(ii) Radical Complexes Derived From Model Compoundsmentioning

confidence: 99%

Understanding natural semiquinone radicals – Multifrequency EPR and relativistic DFT studies of the structure of Hg(II) complexes

2015

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“…OHE 2 thus generated can be transformed to reactive o-semiquinone radicals by a peroxidase/H 2 0 2 -catalyzed reaction [53]. Indeed, the participation of cultured peroxidase-positive astrocytes in the oxidation of catechol estrogens to their respective o-semiquinones has recently been demonstrated through electron spin resonance spectroscopy [54].…”

Section: Mechanism Of Estradiol Neurotoxicitymentioning

confidence: 98%

Pathologic Effect of Estradiol on the Hypothalamus

Brawer

Beaudet

Desjardins

et al. 1993

Biology of Reproduction

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Estradiol provides physiological signals to the brain throughout life that are indispensable for the development and regulation of reproductive function. In addition to its multiple physiological actions, we have shown that estradiol is also selectively cytotoxic to beta-endorphin neurons in the hypothalamic arcuate nucleus. The mechanism underlying this neurotoxic action appears to involve the conversion of estradiol to catechol estrogen and subsequent oxidation to o-semiquinone free radicals. The estradiol-induced loss of beta-endorphin neurons engenders a compensatory increment in mu opioid binding in the medial preoptic area rendering this region supersensitive to residual beta-endorphin or to other endogenous opioids. The consequent persistent opioid inhibition results in a cascade of neuroendocrine deficits that are ultimately expressed as a chronically attenuated plasma LH pattern to which the ovaries respond by becoming anovulatory and polycystic. This neurotoxic action of estradiol may contribute to a number of reproductive disorders in humans and in animals in which aberrant hypothalamic function is a major component.

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“…Catecholamine neurotransmitters such as dopamine may produce semiquinones and quinones via autoxidation, metal ion oxidation and peroxidative enzyme or cytochrome P450 oxidation [92][93][94]. This oxidative process is similar to the one described for the benzene metabolite catechol and the 4-CEs, and it may initiate Parkinson's disease and other neurodegenerative disorders.…”

Section: Unifying Mechanism Of Initiation Of Cancer and Other Diseasesmentioning

confidence: 99%

Initiation of cancer and other diseases by catechol ortho-quinones: a unifying mechanism

Cavalieri

Rogan

Chakravarti

2002

Cellular and Molecular Life Sciences (CMLS)

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Exposure to estrogens is a risk factor for breast and other human cancers. Initiation of breast, prostate and other cancers has been hypothesized to result from reaction of specific estrogen metabolites, catechol estrogen-3,4-quinones, with DNA to form depurinating adducts at the N-7 of guanine and N-3 of adenine by 1,4-Michael addition. The catechol of the carcinogenic synthetic estrogen hexestrol, a hydrogenated derivative of diethylstilbestrol, is metabolized to its quinone, which reacts with DNA to form depurinating adducts at the N-7 of guanine and N-3 of adenine. The catecholamine dopamine and the metabolite catechol (1,2-dihydroxybenzene) of the leukemogen benzene can also be oxidized to their quinones, which react with DNA to form predominantly analogous depurinating adducts. Apurinic sites formed by depurinating adducts are converted into tumor-initiating mutations by error-prone repair. These mutations could initiate cancer by estrogens and benzene, and Parkinson's disease by the neurotransmitter dopamine. These data suggest a unifying molecular mechanism of initiation for many cancers and neurodegenerative diseases and lay the groundwork for designing strategies to assess risk and prevent these diseases.

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Semiquinone Anion Radicals of Catechol(amine)s, Catechol Estrogens, and Their Metal Ion Complexes

Cited by 28 publications

References 64 publications

Understanding natural semiquinone radicals – Multifrequency EPR and relativistic DFT studies of the structure of Hg(II) complexes

Understanding natural semiquinone radicals – Multifrequency EPR and relativistic DFT studies of the structure of Hg(II) complexes

Pathologic Effect of Estradiol on the Hypothalamus

Initiation of cancer and other diseases by catechol ortho-quinones: a unifying mechanism

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