Is spontaneous urinary visible chemiluminescence a reflection of in vivo oxidative stress?

Lissi, E. A.; Salim-Hanna, Marta; Sir, Teresa; Videla, Luis A.

doi:10.1016/0891-5849(92)90118-z

Cited by 31 publications

(19 citation statements)

References 17 publications

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“…This is the first study of the effect of diet on urinary CL levels and corroborates that this parameter can be employed as a complementary index of systemic oxidative stress (20)(21)(22)(23)(24)(25). It can be postulated that this index reflects the excretion of oxidized biomolecular fragments, particularly protein fragments.…”

Section: Resultssupporting

confidence: 59%

“…Furthermore, it has been shown that addition of diethylhydroxyl amine (1 mmol/L) to urine samples does not modify the observed CL (20). All these results rule out the possibility that the large effect of Tempol is due to the products produced in reaction (1).…”

Section: Resultsmentioning

confidence: 54%

“…Among the proposed methodologies can be mentioned those based on the presence of free radical metabolites in biological fluids, particularly in urine (11)(12)(13)(14)(15)(16)(17)(18)(19)). The spontaneous urinary luminescence level has also been proposed as an alternative index of systemic oxidative stress (20)(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

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Spontaneous urinary chemiluminescence and diet. An intervention study in humans

et al. 2001

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Spontaneous urinary visible chemiluminiscence has been measured in samples from a diet intervention study in humans. For a month, two groups, each of 21 male volunteers, received either a Mediterranean-type diet or an occidental (high-fat) diet. Urinary chemiluminescence levels (in 10(3) cpm) were 8.5 +/- 3.1 and 6.0 +/- 2.0 for the high-fat and Mediterranean-type diets, respectively. The differences obtained were statistically significant. These results reflect differences in the oxidative stress associate to both diets and support the proposal that spontaneous urinary chemiluminiscence constitutes a complementary index of systemic oxidative stress.

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Section: Resultssupporting

confidence: 59%

Section: Resultsmentioning

confidence: 54%

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Spontaneous urinary chemiluminescence and diet. An intervention study in humans

et al. 2001

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“…Urinary visible chemiluminescence is a valuable index of systemic oxidative stress in vivo. This is due to the presence of oxidized products, which are generated by lipid peroxidation and decompose in the urine to produce electronically excited molecules that have lifetimes of several hours and emit mostly in the visible region (23,39). We postulate that the enhanced oxidative stress condition observed in our model may contribute to the development of higher levels of BP through an impaired vasodilator tone, presumably by decreasing NO bioavailability.…”

Section: Discussionmentioning

confidence: 78%

Moderate Zinc Deficiency Influences Arterial Blood Pressure and Vascular Nitric Oxide Pathway in Growing Rats

Tomat¹,

Weisstaub²,

Jauregui³

et al. 2005

Pediatr Res

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There is an increasing interest in the involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases. This study was designed to examine whether moderate zinc deficiency during growth influences blood pressure (BP) and vascular nitric oxide (NO) pathway. Three-week-old weaned male Wistar rats were randomly divided into two dietary groups and fed either a moderately zinc-deficient diet (zinc content 9 mg/kg; n ϭ 12) or a control diet (zinc content 30 mg/kg; n ϭ 12) for 60 d. The following were measured: systolic BP, nitrates and nitrites urinary excretion, urinary chemiluminescence intensity, NADPH-diaphorase activity in the thoracic aorta and intestinal arterioles, and NO synthase (NOS) catalytic activity using L-[U14C]-arginine as substrate in the thoracic aorta. Zinc deficiency during growth induced an increase in BP from day 30 of the experimental period, leading to hypertension on day 60. Animals that were fed the zinc-deficient diet had lower urinary excretion levels of nitrates and nitrites and higher intensity of spontaneous luminescence on day 60. At the end of the experiment, zinc-deficient rats showed decreased NADPH diaphorase activity in endothelium and smooth muscle of the thoracic aorta and intestinal arterioles and decreased activity of NOS in thoracic aortic tissue. An imbalance in zinc bioavailability during postnatal and growing periods may be may be a risk factor in development of cardiovascular alterations in adult life. The mechanisms involved may include an impaired vascular NO system as a result of decreased NOS activity and higher systemic oxidative stress. Moderate and marginal zinc deficiency is by far more common than severe deficiency, especially in infants, children, and pregnant women in developing and developed countries, as a result of imbalances between intake and increased requirements (1,2). Zinc is an essential trace element required by all living organisms for many physiologic functions, including growth, development, and reproduction (3). Zinc has been documented to act as an antioxidant, to have membranestabilizing properties, to block apoptotic cell death, and to be essential for endothelial integrity (4 -6). Intracellular zinc is associated with proteins, primarily via complex interactions with cysteines, acting as an integral component of numerous metalloenzymes, structural proteins, and transcription factors (1,7).There is increasing interest in possible involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases (8). Many enzymes that are involved in the regulation of arterial blood pressure (BP), such as nitric oxide (NO) synthase (NOS), angiotensin-converting enzyme, and neutral endopeptidases, contain zinc in their structure (9 -11). The NOSs are a family of enzymes that catalyze the synthesis of NO and L-citrulline from L-arginine in the presence of NADPH and O 2 . The NOS family consists of three isoforms that are expressed in many tissues, including endothelium and vascular

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“…In man, hyperthyroidism is characterized by significant changes in circulating parameters related to oxidative stress, including (i) higher levels of lipid peroxidation indicators (40)(41)(42)(43)(44)(45)(46)(47)(48)(49); (ii) enhancement in hydrogen peroxide and lipid hydroperoxide levels (49); and (iii) diminished levels of antioxidants such as a-tocopherol (41), coenzyme Q (44), ascorbic acid (41), and reduced thiols (42,46,50). These changes correlated with the enhancement in urinary lipid peroxidation products (40) and chemiluminescence response (51) and are either significantly reduced or normalized by thyrostatic therapy or antioxidant supplementation (40-46, 49, 50).…”

Section: T 3 -Induced Enhancement Of Liver O 2 Consumption and Oxidatmentioning

confidence: 95%

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

Videla

2010

IUBMB Life

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SummaryThyroid hormone (L-3,3 0 ,5-triiodothyronine, T 3 ) exerts calorigenic effects by accelerating mitochondrial O 2 consumption through transcriptional activation of respiratory genes, with consequent increased reactive oxygen species (ROS) production. In the liver, ROS generation occurs at different sites of hepatocytes and in the respiratory burst of Kupffer cells, triggering the activation of the transcription factors nuclear factor-jB, signal transducer and activator of transcription 3, and activating protein 1. Under these conditions, the redox upregulation of Kupffer cell-dependent expression of cytokines [tumor necrosis factor-a, interleukin (IL)-1, and IL-6] is achieved, which upon interaction with specific receptors in hepatocytes trigger the expression of antioxidant enzymes (manganese superoxide dismutase, inducible nitric oxide synthase), antiapoptotic proteins (Bcl-2), and acute-phase proteins (haptoglobin, b-fibrinogen). These responses and the promotion of hepatocyte and Kupffer cell proliferation observed represent hormetic effects re-establishing redox homeostasis, promoting cell survival, and protecting the liver against ischemia-reperfusion (IR) injury. It is proposed that hormesis underlying T 3 action may constitute a novel preconditioning strategy for IR injury during liver surgery in man or in liver transplantation using reduced-size grafts from living donors, considering that (i) with the exception of the controversial ischemic preconditioning, all other studied strategies have failed to reach the clinical setting and (ii) T 3 is a well-tolerated therapeutic agent that either lacks major adverse effects or has minimal and controlled side effects. IUBMBIUBMB Life, 62(6): [460][461][462][463][464][465][466] 2010

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Is spontaneous urinary visible chemiluminescence a reflection of in vivo oxidative stress?

Cited by 31 publications

References 17 publications

Spontaneous urinary chemiluminescence and diet. An intervention study in humans

Spontaneous urinary chemiluminescence and diet. An intervention study in humans

Moderate Zinc Deficiency Influences Arterial Blood Pressure and Vascular Nitric Oxide Pathway in Growing Rats

Hormetic responses of thyroid hormone calorigenesis in the liver: Association with oxidative stress

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