The Effects of Hydroxyl Radical Attack on Dopa, Dopamine, 6‐Hydroxydopa, and 6‐Hydroxydopamine

Nappi, Anthony J.; Vass, Emily; Prota, Giuseppe; Memoli, Sofia

doi:10.1111/j.1600-0749.1995.tb00676.x

Cited by 35 publications

(24 citation statements)

References 55 publications

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“…A sensitive and specific salicylate hydroxylation assay was used in conjunction with high performance liquid chromatography with electrochemical detection (HPLC-ED) to monitor 'OH production (Chiueh et al, 1992;Chiueh et al, 1993;Nappi and Vass, 1996;Nappi and Vass, 1997;Nappi and Vass, 1998a;Nappi and Vass, 1998b;Nappi et al, 1999;Nappi et al, 1995). The products of 'OH-mediated salicylate hydroxylation, which include 2,3-and 2,5-dihydroxybenzoic acid (DHBA) and ortho-catechol, were readily detected and measured by HPLC-ED.…”

Section: Hplc-ed Analyses Of "Oh Productionmentioning

confidence: 99%

Hydroxyl radical production by ascorbate and hydrogen peroxide

Nappi

Vass

2000

neurotox res

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Ascorbate (AH') and certain other biological reductants have long been known to produce the cytotoxic hydroxyl radical ('OH) when oxidized by hydrogen peroxide (H202) in the presence of copper or iron catalysts. The present study documents the in vitro production of the "OH solely from the oxidation of AH-by H202, independent of mediation by transition metals. Hydroxyl radical generation resulting from the AH'/H202 system was quantitatively documented by the specific radical-mediated hydroxylation of salicylic acid, a reaction that was readily assayed with HPLC coupled with electrochemical detection. Two ascorbate-copper complexes (e.g., AH-/Cu2+-EDTA/H202 and AH'/Cu2+-EDTA) and a copper/H202 system also generated 'OH, but less effectively than the AH'/H202 system. The ability of AH-and H202 to generate cytotoxic "OH documents a reaction mechanism that may account for cytotoxic activity in some cellular environments where metal catalysts are lacking.

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Section: Hplc-ed Analyses Of "Oh Productionmentioning

confidence: 99%

Hydroxyl radical production by ascorbate and hydrogen peroxide

Nappi

Vass

2000

neurotox res

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“…Because of the unstable nature of the catechol group, it can be oxidized to reactive quinone molecules, which themselves exert toxic effects. Although oxidation of dopamine is primarily mediated via ROS [36], a number of enzymes are able to catalyze dopamine quinone formation, including prostaglandin H synthase, xanthin oxidase and tyrosinase [37]. This auto-oxidation is prevented by antioxidants (e.g.…”

Section: Dopamine: Mechanisms Of Actionmentioning

confidence: 99%

Untitled

et al. 2004

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485 CREB = cAMP responsive element binding protein; IL = interleukin; LPS = lipopolysaccharide; MAO = monamine oxidase; NF-κB = nuclear factor-κB; NO = nitric oxide; PBMC = peripheral blood mononuclear cell; PKA = protein kinase A; ROS = reactive oxygen species; SNS = sympathetic nervous system; TNF = tumour necrosis factor. Available online http://ccforum.com/content/8/6/485 IntroductionThe challenge to the immune system that occurs in endotoxaemia involves stimulation of immune cells to produce large amounts of inflammatory cytokines (e.g. IL-1, IL-6 and tumour necrosis factor [TNF]-α). These mediators stimulate both the hypothalamic-pituitary-adrenal axis and the systemic-adrenomedullary sympathetic nervous system (SNS). Consequently, catecholamines are released from preganglionic efferent and postganglionic SNS fibres, innervating a wide range of target organs and thereby regulating endotoxin-induced alterations in vascular resistance and tone, tissue perfusion, cardiac and renal function, and hormone release. Although dopamine is also released, noradrenaline (norepinephrine) and adrenaline (epinephrine) appear to be the principal neurotransmitters in this respect. In early and late stages of severe inflammation, catecholamine production is significantly increased [1]. Nevertheless, it must be noted that circulating catecholamines are poor markers of SNS activation during acute stress, such as occurs in sepsis [2]. Review Clinical review: Immunomodulatory effects of dopamine in general inflammation AbstractLarge quantitaties of inflammatory mediators are released during the course of endotoxaemia. These mediators in turn can stimulate the sympathetic nervous system (SNS) to release catecholamines, which ultimately regulate inflammation-associated impairment in tissue perfusion, myocardial impairment and vasodilatation. Treatment of sepsis is based on surgical and/or antibiotic therapy, appropriate fluid management and application of vasoactive catecholamines. With respect to the latter, discussions on the vasopressor of choice are ongoing. Over the past decade dopamine has been considered the 'first line' vasopressor and is frequently used to improve organ perfusion and blood pressure. However, a growing body of evidence indicates that dopamine has deleterious side effects; therefore, its clinical relevance seems to be more and more questionable. Nevertheless, it has not been convincingly demonstrated that other catecholamines are superior to dopamine in this respect. Apart from its haemodynamic action, dopamine can modulate immune responses by influencing the cytokine network. This leads to inhibition of expression of adhesion molecules, inhibition of cytokine and chemokine production, inhibition of neutrophil chemotaxis and disturbed Tcell proliferation. In the present review we summarize our knowledge of the immunomodulatory effects of dopamine, with an emphasis on the mechanisms by which these effects are mediated.

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“…In vitro radical generating Fenton system Hydroxyl radicals were generated according to the method of Nappi et al (1995). A mixture of 0.3 mM FeCl 3 , 0.3 mM Na 2 EDTA and 3 mM H 2 O 2 in 5 ml of Tris-buffer adjusted to pH 7.4 in the presence of 0.5 mM salicylic acid was incubated in the dark for 15 min at 37°C.…”

Section: In Vitro Studiesmentioning

confidence: 99%

Effects of nicotine on hydroxyl free radical formation in vitro and on MPTP-induced neurotoxicity in vivo

Ferger

Spratt

Earl

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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Parkinson's disease (PD) is one of the most frequent disorders of the basal ganglia. From epidemiological studies there is a controversial discussion on the question whether tobacco smoking is correlated with a decreased incidence of PD. The present study aimed to elucidate the role of nicotine and its potential neuroprotective effects in a rodent model of PD. These effects may be related to an altered hydroxyl radical formation; this possibility was studied in vitro. Nicotine and alpha-phenyl-N-tert-butyl nitrone (PBN) were examined in a cell-free in vitro Fenton system (Fe3+/EDTA + H2O2) for their radical scavenging properties using the salicylate trapping method. Salicylic acid (0.5 mM) was incubated in the presence and absence of nicotine or PBN and the main products of the reaction of hydroxyl radicals with salicylic acid, namely 2,3- and 2,5-dihydroxybenzoic acid, were immediately determined using HPLC in combination with electrochemical detection. Nicotine and PBN were both able to significantly reduce hydroxyl radical levels at concentrations of 1, 2.5 and 5 mM. Interestingly, at 5 mM nicotine was able to reduce hydroxyl radical levels significantly more than the radical scavenger PBN (5 mM). To investigate the in vivo effects of nicotine, male C57BL/6 mice were used in the MPTP mouse model of PD. Nicotine (0.1 or 0.4 mg/kg s.c.) was administered twice daily for a period of 14 days. On day 8 a single injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg s.c.) was given as well as an enhanced protocol of nicotine treatment (0.1 or 0.4 mg/kg s.c., 30 min before MPTP and 30, 90, 210, 330, 450, 570 min after MPTP) for a total of seven injections of nicotine. High dosage nicotine treatment significantly increased the MPTP-induced loss of body weight and resulted in a significantly decreased striatal dopamine content and an increased dopamine turnover in comparison with the MPTP-treated controls at day 15. However, the lower dosage of nicotine did not significantly alleviate the MPTP-induced effects, although some parameters showed a slight tendency in this direction. These results demonstrate that in vitro nicotine has radical scavenging properties which might suggest neuroprotective effects. In vivo experiments with nicotine, however, showed that a low dosage of nicotine did not alleviate the MPTP-induced dopamine depletion, but a large dosage even enhanced it.

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The Effects of Hydroxyl Radical Attack on Dopa, Dopamine, 6‐Hydroxydopa, and 6‐Hydroxydopamine

Cited by 35 publications

References 55 publications

Hydroxyl radical production by ascorbate and hydrogen peroxide

Hydroxyl radical production by ascorbate and hydrogen peroxide

Untitled

Effects of nicotine on hydroxyl free radical formation in vitro and on MPTP-induced neurotoxicity in vivo

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