Antioxidant activity of albumin-bound bilirubin.

Stocker, Roland; Glazer, Alexander N.; Ames, Bruce N.

doi:10.1073/pnas.84.16.5918

Cited by 670 publications

(441 citation statements)

References 28 publications

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“…Bilirubin, the end product of heme-catabolism also participates in antioxidative machinery of the body, by efficiently scavenging peroxyl radicals and playing the role of a chain breaking antioxidant [32]. The elevated serum levels of bilirubin in schizophrenics are due to possible increased vulnerability of red cell membranes in condition of oxidative stress [33].…”

Section: Discussionmentioning

confidence: 99%

“…The two factors of aging and substance abuse are a reflection of increasing free radical load, where the level of bilirubin decreased in both these conditions contrary to the overall increase in all other groups. Here, it becomes pertinent to mention that bilirubin is transported as albumin bound complex in plasma [32] and it may be possible that the depleting plasma albumin levels are responsible for similar behavior of bilirubin [37].…”

Section: Discussionmentioning

confidence: 99%

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Oxidative Stress-Induced Response of Some Endogenous Antioxidants in Schizophrenia

Dadheech

Sharma

2012

Ind J Clin Biochem

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Oxidative Stress-Induced Response of Some Endogenous Antioxidants in Schizophrenia

Dadheech

Sharma

2012

Ind J Clin Biochem

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“…Bilirubin is the product of haem degradation and has been regarded simply as a waste product of metabolism (Stocker et al, 1987b). Normal plasma concentrations of bilirubin are 5 ± 14 mM and levels exceeding 250 mM are toxic (Stocker et al, 1987b).…”

Section: Discussionmentioning

confidence: 99%

“…Normal plasma concentrations of bilirubin are 5 ± 14 mM and levels exceeding 250 mM are toxic (Stocker et al, 1987b). At normal physiological concentrations in vitro, bilirubin effectively scavenges peroxyl radicals (Stocker et al, 1987a) and reacts with hydroxyl radicals, hydroperoxyl radicals and superoxide anions (Neuzil & Stocker, 1993).…”

Section: Discussionmentioning

confidence: 99%

Low molecular weight plasma antioxidants and lipid peroxidation in maternal and cord blood

et al. 1999

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Objective: To determine the concentrations of the low molecular weight antioxidants urate, bilirubin, albumin and sulphydryl groups and to measure lipid peroxidation levels in pair-matched maternal and cord blood plasma. Design: Venous blood plasma concentrations of urate, bilirubin, albumin and sulphydryls were determined in healthy pregnant women and in pair matched umbilical cords. The ability of maternal and cord plasma to withstand Cu 2 -induced lipid peroxidation was assessed by measuring the production of thiobarbituric acid reactive substances (TBARS) over time in plasma incubated with Cu 2 . Subjects: Forty healthy women, between 10 and 20 weeks gestation, were recruited randomly from an antenatal clinic. Venous blood samples were obtained from the mothers at the recruitment stage and from the umbilical cords of their newborn after delivery. Results: Urate, bilirubin and sulphydryls were present in signi®cantly higher concentrations (P`0.001) in cord plasma than in maternal plasma. Albumin levels were similar in mothers and cords. Signi®cantly lower levels (P 0.018) of TBARS were produced in cord plasma compared with maternal plasma following incubation with Cu 2 . There were signi®cant correlations between albumin and sulphydryl concentrations in maternal plasma (r 0.43, P 0.007) and between urate concentrations in maternal and cord plasma (r 0.37, P 0.026). Conclusion: Urate, bilirubin and sulphydryls are present in signi®cantly higher concentrations in cord blood than in maternal blood. The increased levels of these antioxidants in cord plasma may contribute to the increased resistance of cord plasma to Cu 2 -induced lipid peroxidation.

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“…In all such compounds the structure of the opened 5 tetrapyrrole ring, including the four nitrogens that may serve as potential iron chelation sites, is maintained. Although these bile pigments have been proposed to function as chain-breaking antioxidants [46,47], as will be subsequently shown, they are also excellent iron chelators of the type that both keep iron soluble at near neutral pH and also promote, rather than inhibit, Fenton chemistry. …”

mentioning

confidence: 95%

Free radicals and the etiology of colon cancer

Babbs

1990

Free Radical Biology and Medicine

312

173

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This hypothesis paper reviews diverse evidence suggesting that intracolonic production of oxygen radicals may play a role in carcinogenesis. The hypothesis began to evolve when the author made the chance discovery that 1/10,000 dilutions of feces generated detectable quantities of highly reactive hydroxyl radicals (HO). The rate of HO formation, detected using DMSO as a molecular probe, was quite remarkable, corresponding to that which would be produced by over 10,000 rads of gamma irradiation per day, absorbed in the periphery of the fecal mass adjacent to the mucosa. The relatively high concentrations of iron in feces, together with the ability of bile pigments to act as iron chelators that support Fenton chemistry, may very well permit efficient HO generation from superoxide and hydrogen peroxide produced by bacterial metabolism. Such free radical generation in feces could provide a missing link in our understanding of the etiology of colon cancer: the oxidation of procarcinogens either by fecal HO, or by secondary peroxyl radicals (ROO) to form active carcinogens or mitogenic tumor promotors. Intracolonic free radical formation may explain the high incidence of cancer in the colon and rectum, compared to other regions of the GI tract, as well as the observed correlations of a higher incidence of colon cancer with red meat in the diet, which increases stool iron, and with excessive fat in the diet, which may increase the fecal content of procarcinogens and bile pigments. OVERVIEW OF THE HYPOTHESIS AND RELEVANT CHEMICAL MECHANISMSMy intention in this hypothesis paper is to present a new hypothesis suggesting how oxygen derived free radicals, generated in fecal material next to colonic epithelium, may play a significant role in the etiology of colon cancer. This hypothesis derives from an earlier conjecture by Graf and Eaton [1], coupled with the serendipitous discovery in our laboratory that highly reactive HO radicals can be produced abundantly by suspensions of feces under aerobic conditions. As do many other hypotheses for the pathogenic effects of oxygen centered free radicals in biologic systems [2][3][4][5][6], this one also invokes the superoxide driven Fenton reaction:In feces a ready biologic source of superoxide is the respiratory activity of bacteria [7][8][9][10], notably E. coli [11], perhaps together with spontaneous autoxidation of ferrous iron chelates that have been previously reduced by metabolites of the anerobic subpopulation of fecal flora. Another intriguing source of colonic superoxide is the lipoxygenase activity of normal or sloughed colonic epithelial cells [12]. The necessary iron is provided from the diet, since only a small fraction of dietary iron is absorbed in upper GI tract [13,14]. Hydroxyl (HO) radicals so formed within the colon could easily trigger a variety of carcinogenic mechanisms. For example, they could participate in aromatic hydroxylation reactions [15,16] to form carcinogenic products [17]; they could abstract hydrogen atoms from indoles to form radicals t...

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Antioxidant activity of albumin-bound bilirubin.

Cited by 670 publications

References 28 publications

Oxidative Stress-Induced Response of Some Endogenous Antioxidants in Schizophrenia

Oxidative Stress-Induced Response of Some Endogenous Antioxidants in Schizophrenia

Low molecular weight plasma antioxidants and lipid peroxidation in maternal and cord blood

Free radicals and the etiology of colon cancer

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