Antioxidant behaviour of caffeine: Efficient scavenging of hydroxyl radicals

Shi, Xianglin; Dalal, N. S.; Jain, Abnash C.

doi:10.1016/0278-6915(91)90056-d

Cited by 247 publications

(145 citation statements)

References 32 publications

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“…These alkaloids, in addition to their property of possibly providing metabolic support to the tissue by maintaining adequate levels of cyclic AMP through the inhibition of phosphodiesterase, are also effective scavengers of reactive oxygen, particularly the hydroxyl radicals. 10 The background of this study is provided also by a previous report showing the inhibition of selenite-induced cataract formation by green tea, which is known to be richer in caffeine. 11…”

Section: T Is Well Known That the Pathogenesis Of Cataracts Ismentioning

confidence: 99%

UV-B-Induced Damage to the Lens In Vitro: Prevention by Caffeine

Varma

Hegde

Ковтун

2008

Journal of Ocular Pharmacology and Therapeutics

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Ultraviolet (UV) irradiation is one of the significant risk factors in the genesis of cataracts. Pathogenetically, the process can be triggered by the intraocular generation of various reactive species of oxygen that are well known to be initiated by the penetration of light, especially of the UV frequencies. The contribution of UV exposure in the etiology of this disease is likely to increase further due to ozone depletion in the upper atmosphere. The present studies were undertaken to examine if the UV effects can be attenuated with the xanthine-based alkaloids primarily present in tea and coffee. We have examined this possibility by in vitro lens culture studies with caffeine. As expected, mice lenses incubated in Tyrode solution exposed to UV at 302 nm are physiologically damaged, as evidenced by the inhibition of the active transport of 86 Rb ϩ , an ion acting as a surrogate of the K ϩ . There was a simultaneous decrease in the levels of adenosine triphosphate and glutathione. The addition of caffeine to the medium prevented such deleterious effects. That caffeine and perhaps other xanthinoids have a protective effect against cataract formation induced by UV has hence been demonstrated for the first time. 439

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Section: T Is Well Known That the Pathogenesis Of Cataracts Ismentioning

confidence: 99%

UV-B-Induced Damage to the Lens In Vitro: Prevention by Caffeine

Varma

Hegde

Ковтун

2008

Journal of Ocular Pharmacology and Therapeutics

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“…6), there was little efficacy in inhibition of iNOS. Shi et al (36) demonstrated that caffeine effectively scavenges hydroxy radical (HO⅐) (36). Therefore, this effect of caffeine can be explained by the scavenging of HO⅐ and then inhibition of iNOS protein and nitrite production.…”

Section: Downloaded Frommentioning

confidence: 99%

(−)-Epigallocatechin-3-gallate Blocks the Induction of Nitric Oxide Synthase by Down-Regulating Lipopolysaccharide-Induced Activity of Transcription Factor Nuclear Factor-κB

1997

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SUMMARYNitric oxide (NO) plays an important role in inflammation and multiple stages of carcinogenesis. We investigated the effect of various tea polyphenols and caffeine on the induction of NO synthase (NOS) in thioglycollate-elicited and lipopolysaccharide (LPS)-activated peritoneal macrophages. Gallic acid (GA), (Ϫ)-epigallocatechin (EGC), and (Ϫ)-epigallocatechin-3-gallate (EGCG), the major tea catechin, were found to inhibit inducible NOS (iNOS) protein in activated macrophages. EGCG, a potent antitumor agent with anti-inflammatory and antioxidant properties, inhibited NO generation, as measured by the amount of nitrite released into the culture medium. Inhibition of NO production was observed when cells were cotreated with EGCG and LPS. iNOS activity in soluble extracts of lipopolysaccharide-activated macrophages treated with EGCG (5 and 10 M) for 6 -24 hr was significantly lower than that in macrophages without EGCG treatment. Western blot, reverse transcriptionpolymerase chain reaction, and Northern blot analyses demonstrated that significantly reduced 130-kDa protein and 4.5-kb mRNA levels of iNOS were expressed in lipopolysaccharideactivated macrophages with EGCG compared with those without EGCG. Electrophoretic mobility shift assay indicated that EGCG blocked the activation of nuclear factor-B, a transcription factor necessary for iNOS induction. EGCG also blocked disappearance of inhibitor B from cytosolic fraction. These results suggest that EGCG decreases the activity and protein levels of iNOS by reducing the expression of iNOS mRNA and the reduction could occur through prevention of the binding of nuclear factor-B to the iNOS promoter, thereby inhibiting the induction of iNOS transcription.NO is a short-lived bioactive molecule that participates in the physiology and pathophysiology of many systems (1). NO is synthesized in vivo from L-arginine by NOS with NADPH and oxygen as cosubstrates (2). Molecular cloning and sequencing analyses revealed the existence of at least three main types of NOS isoforms. NOS in the endothelium of blood vessels and brain neurons is constitutive and Ca 2ϩ / calmodulin dependent. This constitutive enzyme synthesizes small amounts of NO triggered by various agonists (e.g., bradykinin, acetylcholine) that increase intracellular Ca 2ϩ . NOS in macrophages and hepatocytes is inducible, not detectable, in unstimulated cells and requires protein synthesis for expression. iNOS produces large amounts of NO several hours after exposure to endotoxin and/or cytokines in macrophages, Kupffer cells, hepatocytes, and fibroblasts. NO has a wide biological role in modulating physiological and pathophysiological processes (1, 3), such as macrophage cytotoxicities, neurotransmissions, neurotoxicities, and regulation of blood pressure. Low concentrations of NO are sufficient, in most cases, to effect these functions. However, during infection and inflammation, in vivo formation of NO is increased, suggesting that NO concentrations are well above those found in normal physiological funct...

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“…The spectrum in Figure 1 c seemed to be a superposition of those from the DMPO adducts of -SO3 and -OH radicals. To test this possibility, we used the well-known reaction of K2Cr2O7 with Na2SO3 to generate the -SO radicals (9,28). As shown in Figure 3a, this reaction generated the typical DMPO/-SO adduct, with hyperfine splittings of aN = 14.7 G and aH = 16.1 G. Figure 1 c.…”

Section: Methodsmentioning

confidence: 99%

Enhanced Generation of Hydroxyl Radical and Sulfur Trioxide Anion Radical from Oxidation of Sodium Sulfite, Nickel(II) Sulfite, and Nickel Subsulfide in the Presence of Nickel(II) Complexes

Shi¹,

Dalal²,

Kasprzak³

1994

Environmental Health Perspectives

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Electron spin resonance (ESR) spin trapping was utilized to investigate the generation of free radicals from oxidation of sodium sulfite, nickel(ll) sulfite, and nickel subsulfide (Ni3S2) by ambient oxygen or H202 at pH 7.4. The spin trap used was 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). Under ambient oxygen, a solution of sodium sulfite alone generated predominantly sulfur trioxide anion radical (-SO0) due to the autoxidation of sulfite.Addition of nickel(ll) chloride [NiOllW] enhanced the -SO; yield about 4-fold. Incubation of sulfite with Ni(ll) in the presence of chelators such asand penicillamine did not have any significant effect on that enhancement. In contrast, albumin, and especially glycylglycylhistidine (GlyGlyHis), augmented the enhancing effect of Ni(ll) by factors of 1.4 and 4, respectively. Computer simulation analysis of the spin-adduct spectrum and formate scavenging experiment showed that the mixture of sodium sulfite, Ni(ll), and GlyGlyHis generated both hydroxyl (-OH) radical and -SO; radical, in the ratio of approximately 1:2. The free-radical spin adduct intensity reached its saturation level in about 5 min. The yield of the radical adducts could be slightly reduced by deferoxamine and very strongly reduced by diethylenetriaminepentaacetic acid (DTPA). Aqueous suspensions of sparingly soluble nickel(ll) sulfite in the presence of air and GlyGlyHis generated surface-located *SO-and 'OH radicals. The same radicals were generated in Ni3S2 suspension in the presence of GlyGlyHis and H202, indicating sulfite production by oxidation of the sulfide moiety of this compound. In view of the present results, the exceptionally high carcinogenic potential of Ni3S2 appears to be due to the ability of both the nickel and sulfide constituents of the molecule to facilitate the generation of genotoxic radicals. -Environ Health Perspect 102 (Suppl 31:91-96 (1994)

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Antioxidant behaviour of caffeine: Efficient scavenging of hydroxyl radicals

Cited by 247 publications

References 32 publications

UV-B-Induced Damage to the Lens In Vitro: Prevention by Caffeine

UV-B-Induced Damage to the Lens In Vitro: Prevention by Caffeine

(−)-Epigallocatechin-3-gallate Blocks the Induction of Nitric Oxide Synthase by Down-Regulating Lipopolysaccharide-Induced Activity of Transcription Factor Nuclear Factor-κB

Enhanced Generation of Hydroxyl Radical and Sulfur Trioxide Anion Radical from Oxidation of Sodium Sulfite, Nickel(II) Sulfite, and Nickel Subsulfide in the Presence of Nickel(II) Complexes

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