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Systemic nitrate and nitrite was circulating among blood, saliva and tissues, after a rich nitrate diet, the nitrate was absorbed and the plasma level peak up in 15-30 minutes with a half-life of about 5-8 hours [3, 21, 22]. As the concentration of nitrate was about 10 times of that in plasma, saliva contained large amount of total nitrate [23]. The active ingestion ability of nitrate in different organs differs greatly, possibly depending on the expression of nitrate transporter protein-sialin [8, 24].
Search results for nitr (15)
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The recycling of dietary nitrate is mainly in salivary glands, where sialin plays a key role in active transport and concentration of nitrate. Part of the nitrate is converted to nitrite by oral bacteria and subsequently absorbed in the stomach and intestine. Nearly 25% of circulating nitrate is reabsorbed by the salivary glands, whereas the majority is excreted by the kidneys. Nitrate performs physiological functions through the exogenous NO3--NO2--NO pathway. NO, nitric oxide; NO2-, nitrite; NO3-, nitrate.
When dietary nitrate is not available, the excretion of total nitrate calculated in health volunteers was much larger than the amount of intake, indicating that nitrate and nitrite could be formed by endogenous synthesis. The endogenous production of nitrate was mainly in intestine mucosa tissues [36]. Nitrate performs physiological functions in various systemic activities, including blood pressure reduction, platelet aggregation inhibition, and vessel protective effect - functions similar to those of NO [3, 37]. Nitrate prevents ischemic heart disease by increasing epicardial blood flow through vasodilation, decreasing vascular resistance, blunting coronary steal, and reducing preload [38]. Dietary nitrate (10 mmol/L soldium nitrate in drinking water) can partly improve age-related hypertension and metabolic activities in mice through a decrease of endogenous NO generation via inhibition of NADPH oxidase and modulation of angiotensin (ANG) II receptor expression [39]. Furthermore, inorganic nitrates suppress (15 mmol/L KNO3) acute and chronic inflammation by raising the neutrophil count, which may reduce the occurrence of atheromatous plaque [40]. Moreover, a long-term dietary nitrate and nitrite deficiency experiment showed that mice would suffer from metabolic syndrome, endothelial dysfunction, and cardiovascular death after 22 months of a low-nitrite/nitrate diet [41]. Inorganic nitrate performs functions of decreasing blood pressure and improving myocardial ischemia by enhancing epithelial cell activity and diastole blood vessels, and reducing platelet aggregation [42].
Nitrates secreted from saliva protect against gastric ulcers by promoting gastric NO expression and stimulating concomitant mucus formation [43]. Stress-induced gastric damage was reported with a water immersion-restraint stress (WIRS) assay in a rat model. Results showed that stress promotes salivary nitrate secretion and nitrite formation in health volunteers, and that exogenous nitrate administration (5 mmol/L NaNO3) recovered gastric mucosal blood flow and introgastric NO level, thereby rescuing the WIRS-induced gastric damage [44]. The concentration of bioactive NO in the stomach increased 50-fold after ingestion of dietary nitrate [45]. Meanwhile, the non-enzymatic production of NO from dietary nitrate (0.1 or 1 mmol/kg NaNO3) could effectively alleviate diclofenac-induced stomach mucosa injury and improve the thickness of slime layer in the stomach [43].
The International Agency for Research on Cancer (IARC) has concluded that there was no substantial evidence implicating nitrates as animal carcinogens in 2010 [56]. Moreover, in recent epidemiological investigations, dietary nitrate showed no association with gastric cancer or esophageal cancer in humans [7, 57]. Some research even showed that nitrate could decrease the occurrence of gastric cancer [11, 58], possibly because the main source of dietary nitrate are vegetables, which contain a large amount of fiber, vitamin C, and other reductants. An investigation in Korea, where the intake of dietary nitrates (390-742 mg/day) is considerably higher than that of European countries (52-156 mg/day) and China (422.8 mg/day), showed that no correlation was found between high intake of nitrate and cancer [59]. Besides, the safety of high dietary nitrate (91 g/L potassium nitrate) supply was identified in a miniature pig model. Liver and kidney tissues were checked after high-dose nitrate feeding for 2 years, and no observed systemic toxicity or damage was found in miniature pigs [60]. With 17 continuous weeks of 85 mg/L sodium nitrate-water supplement, increased insulin sensitivity, decreased plasma IL-10 level, and tendency of pro-long lifetime were found without body injury in these mice [61].
The association of nitrite with cancer seems conflicted [11]. The correlation between nitrite and gastric cancer is contradictory in different epidemiological surveys [57]. In 2011, carrying out a large cohort study including approximately 50000 individuals, followed up on for almost 10 years, Cross and his teammates concluded that nitrate and nitrite were not associated with esophageal or gastric cancer, whereas positive associations were found between red meat intake and esophageal squamous cell carcinoma [62]. Some epidemiological studies use processed or smoked meat as a source of exogenous nitrite ignoring complex compounds such as nitrosamines in such foods, resulting in lack of uniformity and scientific accuracy in conclusions. Therefore, association of exogenous nitrite with cancer seems less likely because large amounts of nitrite are formed endogenously. The nitrite concentration in saliva may rise as high as 72 mg/L after consumption of nitrate equivalent to 200 g of spinach [63]. Besides, people are in contact with nitrosamine in many circumstances, such as through smoke, beer, water, working environment, especially cigarettes which contain about 100-1000 times the level of nitrosamine in the daily diet.
Boxplots of nitrate concentrations in shallow groundwater beneath agricultural and urban land uses, and at depths of private and public drinking water supplies beneath mixed land use. The number of sampled wells were 1573 (agricultural land), 1054 (urban), and 3417 (mixed). The agricultural and urban wells were sampled to assess land use effects, whereas the mixed category wells were sampled at depths of private and public supplies. Median depths of wells in the agricultural, urban, and mixed categories were 34, 32, and 200 feet, respectively. The height of the upper bar is 1.5 times the length of the box, and the lower bound was truncated at the nitrate detection limit of 0.05 mg/L NO3-N.
Due to sparse measurement data, exposures for individuals served by private wells are more difficult to estimate than exposures for those on public water supplies. However, advances in geographic-based modeling efforts that incorporate available measurements, nitrogen inputs, aquifer characteristics, and other data hold promise for this purpose. These models include predictor variables describing land use, nitrogen inputs (fertilizer applications, animal feeding operations), soils, geology, climate, management practices, and other factors at the scale of interest. Nolan and Hitt [40] and Messier et al. [41] used nonlinear regression models with terms representing nitrogen inputs at the land surface, transport in soils and groundwater, and nitrate removal by processes such as denitrification, to predict groundwater nitrate concentration at the national scale and for North Carolina, respectively. Predictor variables in the models included N fertilizer and manure, agricultural or forested land use, soils, and, in Nolan and Hitt [40], water-use practices and major geology. Nolan and Hitt [40] reported a training R2 values of 0.77 for a model of groundwater used mainly for private supplies and Messier, Kane, Bolich and Serre [41] reported a cross-validation testing R2 value of 0.33 for a point-level private well model. These and earlier regression approaches for groundwater nitrate [42,43,44,45,46] relied on predictor variables describing surficial soils and activities at the land surface, because conditions at depth in the aquifer typically are unknown. Redox conditions in the aquifer and the time since water entered the subsurface (i.e., groundwater age) are two of the most important factors affecting groundwater nitrate, but redox constituents typically are not analyzed, and age is difficult to measure. Even if a well has sufficient data to estimate these conditions, the data must be available for all wells in order to predict water quality in unsampled areas. In most of the above studies, well depth was used as a proxy for age and redox and set to average private or public-supply well depth for prediction.
Recent advances in groundwater nitrate exposure modeling have involved machine-learning methods such as random forest (RF) and boosted regression trees (BRT), along with improved characterization of aquifer conditions at the depth of the well screen (the perforated portion of the well where groundwater intake occurs). Tree-based models do not require data transformation, can fit nonlinear relations, and automatically incorporate interactions among predictors [47]. Wheeler et al. [48] used RF to estimate private well nitrate levels in Iowa. In addition to land use and soil variables, predictor variables included aquifer characteristics at the depth of the well screen, such as total thickness of fine-grained glacial deposits above the well screen, average and minimum thicknesses of glacial deposits near sampled wells, and horizontal and vertical hydraulic conductivities near the wells. Well depth, landscape features, nitrogen sources, and aquifer characteristics ranked highly in the final model, which explained 77% and 38% of the variation in training and hold-out nitrate data, respectively.
Under acidic conditions in the stomach, nitrite can be protonated to nitrous acid (HNO2), and subsequently yield dinitrogen trioxide (N2O3), nitric oxide (NO), and nitrogen dioxide (NO2). Since the discovery of endogenous NO formation, it has become clear that NO is involved in a wide range of NO-mediated physiological effects. These comprise the regulation of blood pressure and blood flow by mediating vasodilation [56,57,58], the maintenance of blood vessel tonus [59], the inhibition of platelet adhesion and aggregation [60,61], modulation of mitochondrial function [62] and several other processes [63,64,65,66]. 041b061a72