Zinsser Microbiology

Joklik, Wolfgang K.; Duke, James B.; Smith, David T.; Riley, Harris D.

doi:10.1097/00007611-197306000-00030

Cited by 29 publications

(63 citation statements)

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“…Another ready source of superoxide in the colonic environment is the respiratory activity of bacteria [41][42][43][44], notably catalase negative bacteria and E. coli [45]. Finally, there is also the lipoxygenase activity of normal or sloughed colonic epithelial cells [46], which may provide an additional source of superoxide in the immediate microenvironment of colonic epithelial cells.…”

Section: Sources Of Mucosal Superoxide In Ulcerative Colitismentioning

confidence: 99%

Oxygen radicals in ulcerative colitis

Babbs

1992

Free Radical Biology and Medicine

268

169

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This article reviews the pathophysiologic concept that superoxide and hydrogen peroxide, generated by activated leukocytes, together with low-molecular-weight chelate iron derived from fecal sources and from denatured hemoglobin, amplify the inflammatory response and subsequent mucosal damage in patients with active episodes of ulcerative colitis. The putative pathogenic mechanisms reviewed are as follows: ( l ) Dietary iron is concentrated in fecal material owing to normally limited iron absorption. (2) Mucosal bleeding, characteristic of ulcerative colitis, as well as supplemental oral iron therapy for chronic anemia, further conspire to maintain or elevate mucosal iron concentration in colitis. (3) Fenton chemistry, driven especially by leukocyte-generated superoxide and hydrogen peroxide, leads to formation of hydroxyl radicals. (4) The resultant oxidative stress leads to the extension and propagation of crypt abscesses, either through direct membrane disruption by lipid peroxidation or through generation of secondary toxic oxidants such as chloramines. (5) Chemotactic products of lipid peroxidation, including 4-hydroxynonenal, provide positive feedback to accelerate this inflammatory/oxidative process, leading to acute exacerbations of the disease. (6) Other oxidized products, such as oxidized tryptophan metabolites, created by free radical mechanisms in or near the mucosa, may act as carcinogens or tumor promotors that contribute to the exceedingly high incidence of colon carcinoma in patients suffering from chronic ulcerative colitis. In this way, self-sustaining cycles of oxidant formation may amplify flare-ups of inflammation and mucosal injury in ulcerative colitis. This concept, if proved correct by subsequent research, would provide a rationale for several novel clinical approaches to the management of ulcerative colitis, including use of SOD mimetics, iron chelators, and chain-breaking antioxidants.

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Section: Sources Of Mucosal Superoxide In Ulcerative Colitismentioning

confidence: 99%

Oxygen radicals in ulcerative colitis

Babbs

1992

Free Radical Biology and Medicine

268

169

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“…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].…”

Section: Overview Of the Hypothesis And Relevant Chemical Mechanismsmentioning

confidence: 99%

“…The availability of suitably chelated iron in high concentrations is coupled with the ability of both aerobic and anerobic bacteria to produce superoxide and hydrogen peroxide [7][8][9][10]. Superoxide production by the colonic mucosa itself (exclusive of leukocytes) has been shown to be a potent promotor of mitogenic activity in animal models [12].…”

Section: Integrated Free Radical Hypothesismentioning

confidence: 99%

“…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].…”

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confidence: 99%

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Free radicals and the etiology of colon cancer

Babbs

1990

Free Radical Biology and Medicine

313

176

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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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“…S. saprophyticus has been isolated from 7.1% of rectal swab specimens taken from carcasses of cattle 7 . The organism may be present on normal skin and in the periurethral and urethral region transiently and in small number 8 . Several studies showed that rectal, vaginal, and urethral colonization of S. saprophyticus was associated with UTI caused by this organism 9 .…”

Section: Introductionmentioning

confidence: 99%

Urinary Tract Infections Caused by Staphylococcus saprophyticus and their antimicrobial sensitivity pattern in Young Adult Women

Jhora¹,

Paul²

2011

Bangladesh J Med Microbiol

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The present study was conducted to observe the antibiotic sensitivity pattern of isolated S. saprophyticus from urine samples of patients admitted in inpatient department or visited the out patient department of Sir Salimullah Medical College & Mitford Hospital (SSMC& MH) Dhaka from October 2002 to September 2003. Among the isolates, Esch. coli was the most predominant (82.61%) urinary pathogens followed by S. saprophyticus (7.01%). 93.10% S. saprophyticus was isolated from females of which highest (44.82%) rate of isolation was among female of 18-45 years age group. Rate of isolation was also high (41.38%) among female of <18 years age group. All strains of S. saprophyticus (100%) were sensitive to Imipenem. High sensitivity was also observed to gentamicin (86.20%) and ceftriaxone (72.41%). Ciprofloxacin was found to be sensitive against 68.96% isolates. Sensitivity of ceftazidime, cephalexin and cloxacillin were 65.51%, 55.17% and 55.17% respectively. However, most of the S. saprophyticus are resistant to ampicillin, nalidixic acid and cotrimoxazole. So, the present study illustrates that physicians and microbiologists must be aware that S saprophyticus is an important cause of UTIs in young women and there is a need for continuous evaluation of common antibiotics used in the therapy of uropathogens.

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Zinsser Microbiology

Cited by 29 publications

References 0 publications

Oxygen radicals in ulcerative colitis

Oxygen radicals in ulcerative colitis

Free radicals and the etiology of colon cancer

Urinary Tract Infections Caused by Staphylococcus saprophyticus and their antimicrobial sensitivity pattern in Young Adult Women

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