The beneficial and hazardous effects of simple phenolic compounds

Stich, H. F.

doi:10.1016/0165-1218(91)90125-6

Cited by 169 publications

(73 citation statements)

References 98 publications

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“…Butylated hydroxyanisole and butylated hydroxytoluene, lipophilic agents that freely cross the membrane and scavenge intracellular free radicals, caused even further cell death (463 Ϯ 50 and 462 Ϯ 17%, respectively). These phenolic agents, however, caused significant cell death when administered alone at concentrations as low as 25 and 50 M, respectively (data not shown), as has been demonstrated to occur in some conditions (reviewed by Stich, 1991). Melatonin, which is effective in removing intracellular reactive oxygen species, was also not protective (265 Ϯ 11%).…”

Section: Bh4 Causes Catecholamine Cell-specific Death 635mentioning

confidence: 86%

Tetrahydrobiopterin Is Released from and Causes Preferential Death of Catecholaminergic Cells by Oxidative Stress

et al. 2000

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The underlying cause of the selective death of the nigral dopaminergic neurons in Parkinson's disease is not fully understood. Tetrahydrobiopterin (BH4) is synthesized exclusively in the monoaminergic, including dopaminergic, cells and serves as an endogenous and obligatory cofactor for syntheses of dopamine and nitric oxide. Because BH4 contributes to the syntheses of these two potential oxidative stressors and also undergoes autoxidation, thereby producing reactive oxygen species, it was possible that BH4 may play a role in the selective vulnerability of dopaminergic cells. BH4 given extracellularly was cytotoxic to catecholamine cells CATH.a, SK-N-BE(2)C, and PC12, but not to noncatecholamine cells RBL-2H3, CCL-64, UMR-106-01, or TGW-nu-1. This was not caused by increased dopamine or nitric oxide, because inhibition of their syntheses did not attenuate the damage and BH4 did not raise their cellular levels. Dihydrobiopterin and biopterin were not toxic, indicating that the fully reduced form is responsible. The toxicity was caused by generation of reactive oxygen species, because catalase, superoxide dismutase, and peroxidase protected the cells from the BH4-induced demise. Furthermore, thiol agents, such as reduced glutathione, dithiothreitol, ␤-mercaptoethanol, and N-acetylcysteine were highly protective. The BH4 toxicity was initiated extracellularly, because elevation of intracellular BH4 by sepiapterin did not result in cell damage. BH4 was spontaneously released from the cells of its synthesis to a large extent, and the release was not further enhanced by calcium influx. This BH4-induced cytotoxicity may represent a mechanism by which selective degeneration of dopaminergic terminals and neurons occur.

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Section: Bh4 Causes Catecholamine Cell-specific Death 635mentioning

confidence: 86%

Tetrahydrobiopterin Is Released from and Causes Preferential Death of Catecholaminergic Cells by Oxidative Stress

et al. 2000

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“…This compound is found in edible vegetables, fruits and nuts (Masella et al, 1999), brown rice (Hudson et al, 2000) and pecans (Stich, 1991), in plant-derived beverages like tea (Yen and Hsieh, 2000), Hibiscus sabdariffa (Tseng et al, 1996) and white grape wine (Li et al, 1993), and in herbal medicines (Liu et al, 1992;Lee and Yang, 1994) and exerts contradictory biologic effects. Studies in animals have recently shown PCA to be effective in inhibiting the carcinogenic action of diethylnitrosamine in the liver (Tanaka et al, 1993), azoxymethane in the colon (Kawamori et al, 1994), N-nitrosobis(2-oxopropyl)amine in pancreas (Nakamura et al, 2000) and N-methyl-N-nitrosourea in glandular stomach tissue (Tanaka et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Protocatechuic acid inhibits cancer cell metastasis involving the down‐regulation of Ras/Akt/NF‐κB pathway and MMP‐2 production by targeting RhoB activation

Lin

Chen

Chou

et al. 2010

British J Pharmacology

107

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BACKGROUND AND PURPOSEProtocatechuic acid (PCA) is plentiful in edible fruits and vegetables and is thus one anti-oxidative component of normal human diets. However, the molecular mechanisms involved in the chemopreventive activity of PCA are poorly understood. Here, we investigated the mechanism(s) underlying the anti-metastatic potential of PCA. EXPERIMENTAL APPROACHWe used AGS cells in a wound healing model and Boyden chamber assays in vitro and injection of B16/F10 melanoma cells in mice (metastasis model in vivo) to analyse the effect of PCA on cancer cell invasion and metastasis. The activities and expression of molecular proteins were measured by zymographic assay, real-time RT-PCR and Western blotting. KEY RESULTSPCA inhibited cell migration and invasion at non-cytotoxic concentrations. Decreased expression of matrix metalloproteinase (MMP)-2 and a coincident increase in tissue inhibitor of MMP followed treatment with PCA. The PCA-inhibited MMP-2 activity and expression was accompanied by inactivation of NF-kB. All these effects of PCA could be mediated via the RhoB/ protein kinase Ce (PKCe) and Ras/Akt cascade pathways, as demonstrated by inhibition of PKCe and transfection of PKCe siRNA and ras overexpression vector. Finally, PCA inhibited metastasis of B16/F10 melanoma cells to the liver in mice. CONCLUSION AND IMPLICATIONSOur data imply that PCA down-regulated the Ras/Akt/NF-kB pathway by targeting RhoB activation, which in turn led to a reduction of MMP-mediated cellular events in cancer cells and provides a new mechanism for the anti-cancer activity of PCA. Abbreviations

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“…Это же в полной мере относится к производным 1,4 ДГП. Множественные механизмы, также как и спе цифичность действия природных и синтетических анти оксидантов, приводящая к варьированию профиля био логической активности от антимутагенности до ко му тагенности, подробно обсуждались ранее [8, 15,40,122,138]. Эти проблемы не теряют своей актуальности и применительно к антиканцерогенам [90].…”

Section: влияние антимутагенов на молекулярные события критические дunclassified

Molecular basis of applying antimutagens as anticarcinogens

Гончарова

Иосифовна²,

Kuzhir

et al. 2005

Ecological genetics

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The paper presents a review of current data on mechanisms of natural and synthetic antimutagen action underlying the expediency and availability of their application as anticarcinogens. Previously, some molecular processes involved in carcinogenesis as well as some therapeutic targets are considered. The effects of antimutagens on those or other molecular targets have been summarized in table. Along with the literature data on plant antimutagens, some experimental results and supposed mechanisms of the 1,4-dihydropyridine derivatives have been analyzed.

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The beneficial and hazardous effects of simple phenolic compounds

Cited by 169 publications

References 98 publications

Tetrahydrobiopterin Is Released from and Causes Preferential Death of Catecholaminergic Cells by Oxidative Stress

Tetrahydrobiopterin Is Released from and Causes Preferential Death of Catecholaminergic Cells by Oxidative Stress

Protocatechuic acid inhibits cancer cell metastasis involving the down‐regulation of Ras/Akt/NF‐κB pathway and MMP‐2 production by targeting RhoB activation

Molecular basis of applying antimutagens as anticarcinogens

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