The Effect of Nitric Oxide on Bacteria

Shank, J. L.; Silliker, J. H.; Harper, Rachel

doi:10.1128/am.10.3.185-189.1962

Cited by 54 publications

(22 citation statements)

References 16 publications

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“…Data from these studies had shown that the ability of sodium nitrite to kill and to inhibit certain microorganisms was pH dependent, reaching a maximum at the pH range of 4.5-5.5 (24,39). The reactive nitrogen species directly responsible for the toxicity had been proposed to be NO/NOz or HNO2 (24,40). Data from the present study indicate that sodium nitrite effectively killed virulent M. tuberculosis at acidic pH (Table 2).…”

Section: Discussionmentioning

confidence: 48%

“…The effector molecules mediating mycobacteriocidal activity that result from acidification of NO2-could be either NO, NO2, or HNOz, or any combination of the three. The antibacterial effect of sodium nitrite, a compound that can form various oxides of nitrogen at acidic pH (12,24), has been known for years (39). The mechanisms for this effect had been studied extensively in the past as a result of the widespread use of NO2-in meat curing.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms for this effect had been studied extensively in the past as a result of the widespread use of NO2-in meat curing. Data from these studies had shown that the ability of sodium nitrite to kill and to inhibit certain microorganisms was pH dependent, reaching a maximum at the pH range of 4.5-5.5 (24,39). The reactive nitrogen species directly responsible for the toxicity had been proposed to be NO/NOz or HNO2 (24,40).…”

Section: Discussionmentioning

confidence: 99%

“…shown that NO2-is tumoristatic at low pH, apparently due to the formation of nitrous acid (pK~ = 3.4), which then dismutates to generate NO and NO2 (12,24). Therefore, to examine directly the antimycobacterial effect of RNI, we tested the effect of N02-on M. tuberculosis at various pHs.…”

Section: Acidified No2-is Mycobacteriocidal Recent Reports Havementioning

confidence: 99%

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Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

Chan

Xing

Magliozzo

et al. 1992

The Journal of Experimental Medicine

939

700

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Sllmmal~Tuberculosis remains one of the major infectious causes of morbidity and mortality in the world, yet the mechanisms by which macrophages defend against Mycobacterium tuberculosis have remained obscure. Results from this study show that murine macrophages, activated by interferon % and lipopolysaccharide or tumor necrosis factor or, both growth inhibit and kill M. tuberculosis. This antimycobacterial effect, demonstrable both in murine macrophage cell lines and in peritoneal macrophages of BALB/c mice, is independent of the macrophage capacity to generate reactive oxygen intermediates (ROI). Both the ROI-deficient murine macrophage cell line Dg, and its ROI-generating, parental line J774.16, expressed comparable antimycobacterial activity upon activation. In addition, the oxygen radical scavengers superoxide dismutase (SOD), catalase, mannitol, and diazabicyclooctane had no effect on the antimycobacterial activity of macrophages. These findings, together with the results showing the relative resistance of M. tuberculosis to enzymaticaUy generated H202, suggest that ROI are unlikely to be significantly involved in killing M. tuberculosis. In contrast, the antimycobacterial activity of these macrophages strongly correlates with the induction of the t-arginine-dependent generation of reactive nitrogen intermediates (RNI). The effector molecule(s) that could participate in mediating this antimycobacterial function are toxic RNI, including NO, NO2, and HNO2, as demonstrated by the micobacteriocidal effect of acidified NO2. The oxygen radical scavenger SOD adventitiously perturbs RNI production, and cannot be used to discriminate between cytocidal mechanisms involving ROI and RNI. Overall, our results provide support for the view that the r-arginine-dependent production of RNI is the principal effector mechanism in activated murine macrophages responsible for killing and growth inhibiting virulent M. tuberculosis.

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Acidified No2-is Mycobacteriocidal Recent Reports Havementioning

confidence: 99%

See 2 more Smart Citations

Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

Chan

Xing

Magliozzo

et al. 1992

The Journal of Experimental Medicine

939

700

View full text Add to dashboard Cite

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“…This confirmed a previous report (6) that induction of the MO N02--producing pathway correlates with and is required for cytostasis in this system . Since N02-can be growth inhibitory (13)(14)(15)(16), we tested if exogenous NaN02 could cause cytostasis in the cocultures. NaN03 served as a control.…”

Section: N02 -Synthesis (O) and [ 3 H]mentioning

confidence: 99%

Nitric oxide. A macrophage product responsible for cytostasis and respiratory inhibition in tumor target cells.

Stuehr

Nathan

1989

The Journal of Experimental Medicine

1,622

771

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Once activated by agents such as IFN-y and bacterial LPS, macrophages (MO)t can inhibit the growth of a wide variety of tumor and microbial targets (1, 2) . Although MO products such as hydrogen peroxide, TNFa, and IL-1 cause cytostasis and/or cytotoxicity (3-5), in many cases these mediators do not appear to be involved . With some targets, Mo-mediated cytostasis and injury to the mitochondria) electron transport chain (METC) require a process associated with MO oxidation of the guanido nitrogens of L-arginine to N02 -/NO3 -(6). However, it is unknown if a metabolite of L-arginine causes these injuries, and if so, which metabolite. Activated Mo have recently been shown to release a compound similar to or identical with the reactive radical nitric oxide (NO .) during metabolism of L-arginine to N02 -/NO3 -(7). This report identifies NO. (or a closely related product) as a mediator of MO-induced cytostasis and mitochondria) respiratory inhibition in lymphoma cells . Materials and MethodsReagents. Cells were cultured in minimum Eagle's medium, a modification (aMEM) or RPMI 1640 (RPMI ; KC Biological Inc ., Lenexa, KS), both supplemented with 8% bovine calf serum (CS; HyClone Systems, Logan, UT), L-glutamine (584 mg/liter), penicillin (50 U/ml), and streptomycin (50 pg/ml) . Catalase and N°-monomethyl-L-arginine (NMA) were from Calbiochem-Behring Corp. La Jolla, CA. NO . gas (99% pure) and N2 gas (45 ppm 02) were from Matheson Gas Products, East Rutherford, NJ . [Methyl-3 H]TdR (2 Ci/mmol) was from New England Nuclear, Boston, MA. Pure IFN-y was generously provided by Genentech, South San Francisco, CA . LPS (Escherichia coli serotype 0127 : B8) and all other reagents were from Sigma Chemical Co., St . Louis, MO. Concentrated stock solutions were prepared in culture medium (for myoglobin, ascorbate, catalase, NMA, LPS, and IFN-y) or saline (for NaN02, NaN03, FeS04) and sterile filtered (0 .22 pm, Millipore, Danvers, MA) .

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The Color of Meat

Pegg

Shahidi

2004

Nitrite Curing of Meat

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The Effect of Nitric Oxide on Bacteria

Cited by 54 publications

References 16 publications

Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

Nitric oxide. A macrophage product responsible for cytostasis and respiratory inhibition in tumor target cells.

The Color of Meat

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