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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A chemiluminescence (CL) assay has been used to measure the reactive oxygen species (ROS)-generating capacity of phagocytes. Primed neutrophils produce ROS and nitric oxide (NO) upon induction of nitric oxide synthase (NOS) activity. NO and superoxide (O(2)(-)) form peroxynitrite (ONOO(-)), and emit CL. We examined the involvement of NOS in the CL response of neutrophils using a method based on the modulation of enzyme activity of NOS by the substrate L-arginine and an inhibitor; L-
NAME
. We used lipopolysaccharide (LPS) as the neutrophil-priming agent. Addition of sodium azide (
NaN
(3)) with horseradish peroxidase (HRP) to luminol-dependent CL, gave a CL response that was significantly enhanced when 10 mmol/L L-arginine was present (p <0.05), suggesting that NOS activity contributed to the CL response of human neutrophils. LPS-primed luminol-dependent CL was significantly inhibited by L-
NAME
compared with D-
NAME
. The proportion of the difference between the two inhibitors in luminol-dependent CL was 12.3 +/- 15.0%. Therefore, approximately 12% of the LPS-primed luminol-dependent CL decrease induced by L-
NAME
indicated the contribution of NOS activity to the CL response.
...
PMID:Contribution of nitric oxide synthase to human neutrophil chemiluminescence. 1060 4
Residual oil fly ash (ROFA) is a pollutant dust that stimulates production of reactive oxygen species (ROS) from mitochondria and apoptosis in alveolar macrophages (AM), but the relationship between these two processes is unclear. In this study, human AM were incubated with ROFA or vanadyl sulfate (VOSO(4)), the major metal constituent in ROFA, with or without nitro-L-arginine methyl ester (L-
NAME
), diphenyleneiodonium (DPI), and mitochondrial electron transport inhibitors. Interactions among production of ROS, nitric oxide (NO), and apoptosis of AM were determined. ROFA-stimulated ROS production was attenuated by DPI, rotenone, antimycin, and
NaN
(3), but not by L-
NAME
, a pattern mimicked by VOSO(4). ROFA-induced apoptosis was inhibited by L-
NAME
and a caspase-3-like protease inhibitor, but not by mitochondrial inhibitors. ROFA enhanced NO-mediated increase in caspase-3-like activity. VOSO(4) had minor effects on apoptosis. Thus ROFA-stimulated production of ROS from mitochondria was independent of apoptosis of AM, which was mediated by activation of caspase-3-like proteases and NO. The pro-oxidant effect but not the proapoptotic effect of ROFA was mediated by vanadium.
...
PMID:Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage. 1238 87
Hypothermic perfusion of the heart decreases oxidative phosphorylation and increases NADH. Because O(2) and substrates remain available and respiration (electron transport system, ETS) may become impaired, we examined whether reactive oxygen species (ROS) exist in excess during hypothermic perfusion. A fiberoptic probe was placed on the left ventricular free wall of isolated guinea pig hearts to record intracellular ROS, principally superoxide (O(2)(-).), and an extracellular reactive nitrogen reactant, principally peroxynitrite (ONOO(-)), a product of nitric oxide (NO.) + O(2)(-). Hearts were loaded with dihydroethidium (DHE), which is oxidized by O(2)(-). to ethidium, or were perfused with l-tyrosine, which is oxidized by ONOO(-) to dityrosine (diTyr). Shifts in fluorescence were measured online; diTyr fluorescence was also measured in the coronary effluent. To validate our methods and to examine the source and identity of ROS during cold perfusion, we examined the effects of a superoxide dismutase mimetic Mn(III) tetrakis(4-benzoic acid)porphyrin chloride (MnTBAP), the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-
NAME
), and several agents that impair electron flux through the ETS: menadione, sodium azide (
NaN
(3)), and 2,3-butanedione monoxime (BDM). Drugs were given before or during cold perfusion. ROS measured by DHE was inversely proportional to the temperature between 37 degrees C and 3 degrees C. We found that perfusion at 17 degrees C increased DHE threefold versus perfusion at 37 degrees C; this was reversed by MnTBAP, but not by l-
NAME
or BDM, and was markedly augmented by menadione and
NaN
(3). Perfusion at 17 degrees C also increased myocardial and effluent diTyr (ONOO(-)) by twofold. l-
NAME
, MnTBAP, or BDM perfused at 37 degrees C before cooling or during 17 degrees C perfusion abrogated, whereas menadione and
NaN
(3) again enhanced the cold-induced increase in ROS. Our results suggest that hypothermia moderately enhances O(2)(-). generation by mitochondria, whereas O(2)(-). dismutation is markedly slowed. Also, the increase in O(2)(-). during hypothermia reacts with available NO. to produce ONOO(-), and drug-induced O(2)(-). dismutation eliminates the hypothermia-induced increase in O(2)(-).
...
PMID:Hypothermia augments reactive oxygen species detected in the guinea pig isolated perfused heart. 1464 63
Possible regulation of salt stress-induced ABA accumulation by nitric oxide (NO) in maize seedling was investigated. Both NO and ABA contents of maize leaves and root tips were increased in response to salt stress (Fig.1,2). Similar to the effects of salt stress, ABA contents of maize leaves and root tips were increased after the treatment of maize leaves with sodium nitroprusside (SNP, a nitric oxide donor) alone (Fig.3). Compared to the salt stress-induced ABA accumulation, this SNP-induced ABA increase was much faster, suggesting that NO may be an intermediate signal from salt stress to ABA accumulation. When NO production inhibitors L-
NAME
and
NaN
(3) treatments were applied, salt stress-induced ABA accumulation was lowered (Fig.4). Treatment with NO scavenger cPTIO also inhibited the salt stress-induced ABA increase (Fig.5). From these results it is deduced that NO is involved in regulation of ABA accumulation under salt stress.
...
PMID:[Involvement of nitric oxide in regulation of salt stress-induced ABA accumulation in maize seedling]. 1707 82
The features of neuronal damage induced by the mitochondrial toxin
NaN
(3) were investigated in rat primary cortical neuron cultures. Cell viability (MTT colorimetric determination) and transmembrane mitochondrial potential (J-C1 fluorescence) were concentration-dependently reduced 24 h after
NaN
(3); neither nuclear fragmentation by DAPI, nor Annexin V positivity by flow cytometry were detected, ruling out the occurrence of apoptosis. The loss in cell viability (to 54 +/- 2%) observed 24 h after a 10-min treatment with 3 mM
NaN
(3) was prevented by the NMDA glutamate receptor antagonist MK801 (1 microM), by the antioxidants trolox (100 microM) and acetyl-L-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-
NAME
(100 microM), but not by the guanylylcyclase inhibitor ODQ, 10 microM. The mitochondrial dysfunction induced by
NaN
(3) provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for screening potential protective agents against neuronal death.
...
PMID:Sodium azide induced neuronal damage in vitro: evidence for non-apoptotic cell death. 1884 70
Low light intensity is common in northern China due to fog or haze, and causes stress for crop plants. To solve the problem of low light intensity stress on the growth and development of vegetable crops in China, new cropping strategies must be developed. We previously showed that an appropriate ratio of ammonium and nitrate (NH
4
+
:NO
3
-
) can alleviate the effect of low light stress on plants, although it is not clear what mechanism is involved in this alleviation. We propose the hypothesis that an appropriate ammonium/nitrate ratio (10:90) can induce NO synthesis to regulate the AsA-GSH cycle in mini Chinese cabbage seedlings under low light intensity. To test the hypothesis, we conducted a series of hydroponic experiments. The results indicated that, under low light intensity conditions, appropriate NH
4
+
:NO
3
-
(N, NH
4
+
:NO
3
-
= 10:90) decreased the contents of malondialdehyde (MDA), hydrogen peroxide (H
2
O
2
), and superoxide anion (O
2
-
) in leaves compared with nitrate treatment. Exogenous nitric oxide (SNP) had the same effects on MDA, H
2
O
2
, and O
2
-
. However, with the addition of a NO scavenger (hemoglobin, Hb) and NO inhibitors (N-nitro-l-arginine methyl ester, L-
NAME
),
NaN
3
(NR inhibitor) significantly increased the contents of MDA, H
2
O
2
, and O
2
-
. The application of N solution enhanced the AsA-GSH cycle by increasing the activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), and ascorbate oxidase (AAO), compared with control (NH
4
+
:NO
3
-
= 0:100). Meanwhile, exogenous SNP significantly increased the above indicators. All these effects of N on AsA-GSH cycle were inhibited by the addition of Hb, L-
NAME
and
NaN
3
in N solution. The results also revealed that the N and SNP treatments upregulated the relative expression level of
GR, MDHAR1, APXT, DHAR2
, and
AAO
gene in mini Chinese cabbage leaves under low light stress. These results demonstrated that the appropriate NH
4
+
:NO
3
-
(10:90) induced NO synthesis which regulates the AsA-GSH cycle in mini Chinese cabbage seedlings under low light stress.
...
PMID:Nitric Oxide Is Involved in the Regulation of the Ascorbate-Glutathione Cycle Induced by the Appropriate Ammonium: Nitrate to Mitigate Low Light Stress in
Brassica pekinensis
. 3171 21
