Borate Ameliorates Sodium Nitrite-Induced Oxidative Stress Through Regulation of Oxidant/Antioxidant Status: Involvement of the Nrf2/HO-1 and NF-κB Pathways.

The widespread industrial use of nitrite in preservatives, colorants, and manufacturing rubber products and dyes increases the possibilities of organ toxicity. Lithium borate (LB) is known as an antioxidant and an oxidative stress reliever. Therefore, this study is aimed at examining the effect of LB on nitrite-induced hepatorenal dysfunction. Twenty-eight male Swiss mice were divided into four equal groups. Group 1, the control group, received saline. Group 2 received LB orally for 5 consecutive days at a dose of 15 mg/kg bw. Group 3, the nitrite group, received sodium nitrite (NaNO2) on Day 5 (60 mg/kg bw intraperitoneally). Group 4, the protective group (LB + NaNO2 group), received LB for 5 days and then a single dose of NaNO2 intraperitoneally on Day 5, the same as in Groups 2 and 3, respectively. Samples of blood and kidney were taken for serum analysis of hepatorenal biomarkers, levels of antioxidants and cytokines, and the expression of genes associated with oxidative stress and inflammation. NaNO2 intoxication increased markers of liver and kidney functions yet decreased reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities in blood. NaNO2 also increased the expression of tumor necrosis factor (TNF-α), interleukin-1ß and interleukin-6 (IL-1ß and IL-6). Pre-administration of LB protected mice from oxidative stress, lipid peroxidation, and the decrease in antioxidant enzyme activity. Moreover, LB protected mice from cytokine changes, which remained within normal levels. LB ameliorated the changes induced by NaNO2 on the mRNA of nuclear factor erythroid 2-related factor 2 (Nfr2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB), transforming growth factor-beta 2 (TGF-ß2), and glutathione-S-transferase (GST) as determined using quantitative real-time PCR (qRT-PCR). These results collectively demonstrate that LB ameliorated NaNO2-induced oxidative stress by controlling the oxidative stress biomarkers and the oxidant/antioxidant state through the involvement of the Nrf2/HO-1 and NF-κB signaling pathways.

Effects of adding sodium nitrite and tea polyphenols on the characterizations and cytotoxicity of carbon nanoparticles from fried pork.

Carbon nanoparticles (CNPs) extensively present in thermal-processed foods. Sodium nitrite (NaNO2) and tea polyphenols (TP) are commonly used in meat processing, while the properties and cytotoxicity of CNPs existed in fried pork added NaNO2 and TP remain unknown. The results showed that compared with no addition (NA, 4.008 ± 0.43 nm) in soaked pork, the smaller diameters of CNPs (0.968 ± 0.44 nm) were found in CNPs-NaNO2-20 group (addition 20 mg/kg NaNO2), the larger (155.8 ± 7.30 nm) in CNPs-TP-100 group (addition 100 mg/kg TP). The diameter of CNPs was positively correlated with the added concentration. CNPs decreased the viability of HL-7702 cells. Compared with NA group, cell viability in CNPs-NaNO2-80 group was obviously (p < 0.05) decreased by 3.17%, while the CNPs-TP-200 group was 13.84% higher. CNPs could block cells growth by arresting cells in S-phase and increasing cellular ROS levels. CNPs generated in fired pork added 200 mg/kg TP in soaking showed less cytotoxicity.

Hesperidin prevents the combined toxicity of decabromodiphenyl ether and sodium nitrite in vitro.

Decabromodiphenyl ether (BDE-209) and Sodium nitrite (SN) coexist in the processing meat and fish foods, but there is no research considering them together. The present study aimed to investigate the binary mixture's toxicity of BDE-209 and SN and explore the protective effect of hesperidin (Hsp) on the combined toxicity. Results showed that compared with the impact of BDE-209 or SN alone, the binary mixture had a synergistic toxic effect on impairing the viability of HepG2 cells, accompanied by oxidative stress, Ca2+ accumulation, mitochondrial dysfunction. The increase of γ-H2AX fluorescent foci and micronuclei number also indicated its genotoxicity. Pretreatment of Hsp could significantly alleviate the above damage caused by the binary combination. These findings revealed the toxicological interaction of BDE-209 and SN and highlighted that food containing abundant natural flavonoids, as hesperidin, could reduce this toxicological risk.

Toxicity of sodium nitrite-based vertebrate pesticides for European starlings (Sturnus vulgaris).

In the 21st century, invasive animals rank second only to habitat destruction as the greatest threat to global biodiversity. Socially-acceptable and cost-effective strategies are needed to reduce the negative economic and environmental impacts of invasive animals. We investigated the potential for sodium nitrite (SN; CAS 7632-00-0) to serve as an avian toxicant for European starlings (Sturnus vulgaris L.). We also assessed the non-target hazard of an experimental formulation of SN that is being developed as a toxicant for invasive wild pigs (Sus scrofa L.). In gavage experiments with European starlings, we identified a lowest observed adverse effect level (LOAEL) for mortality of 2.40% technical SN (w/v; 120 mg SN/kg body mass) and a no observed adverse effect level (NOAEL) for mortality of 1.30% technical SN (65 mg/kg). The exposure of ten starlings to the experimental formulation of SN (10% SN pig toxicant) resulted in one starling mortality during four days of exposure to the toxic bait. Sodium nitrite toxicity presented a moderate hazard to European starlings; thus, the future development of SN as an avian toxicant is dependent upon its cost-effectiveness. We discuss the management of toxic effects and non-target hazards of SN for wild birds, including best practices for toxic baiting of vertebrate pests and management of invasive wild pigs.

BaZiBuShen alleviates altered testicular morphology and spermatogenesis and modulates Sirt6/P53 and Sirt6/NF-κB pathways in aging mice induced by D-galactose and NaNO2.

ETHNOPHARMACOLOGICAL RELEVANCE: Sperm infertility and testicular atrophy are symptoms associated with aging. BaZiBuShen formula (BZBS), a patented Chinese herbal prescription composed of Semen Cuscutae, Fructus Lycii, Epimedii Folium, Fructus Schisandrae Sphenantherae, Fructus Cnidii, Fructus Rosae Laevigatae, Semen Allii Tuberosi., Radix Morindae Officinalis, Herba Cistanches, Fructus Rubi, Radix Rehmanniae Recens, Radix Cyathulae, Radix Ginseng, Cervi Cornu Pantotrichum, Hippocampus, and Fuctus Toosendan, has been used as a kidney-tonifying and anti-aging drug as well as for the treatment of impotence and male infertility in traditional Chinese medicine. AIM OF THE STUDY: We aimed at investigating whether BZBS preserves sperm and testes morphology in aging mice, and to explore the underlying mechanisms. MATERIALS AND METHODS: BZBS was orally administered to aging mice induced by D-galactose (D-gal) and NaNO2 for 65 days. Sperm quality and testes pathophysiological alterations were examined by a Semen Analysis System, hematoxylin-eosin staining, transmission electron microscopy, and mitochondrial complex IV activity. In addition, serum levels of total antioxidant capacity (TAC), malondialdehyde (MDA), 8-hydroxy-desoxyguanosine (8-OH-dG), reduced glutathione (GSH), oxidized glutathione disulfide (GSSG), testosterone (T), follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2) and tumor necrosis factor-α (TNF-α) were determined by ELISA. The expressions of P450 aromatase (CYP19), sirtuin 6 (Sirt6), P53, inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB)-p65, and phospho-NF-κB-p65 (NF-κB-pp65) in the testes were examined by western blot and/or immunohistochemical staining. RESULTS: Sustained exposure to D-gal/NaNO2 caused a deterioration of sperm quality and testes morphology in this rapid aging mouse model. BZBS treatment curtailed these alterations. These beneficial effects were associated with increased serum levels of TAC, GSH/GSSG, T, E2, and FSH, and decreased levels of MDA, TNF-α, and 8-OH-dG. BZBS treatment also downregulated the expressions of P53, iNOS, and NF-κB-pp65, as well as upregulated the expressions of Sirt6 and CYP19 in aging testes. CONCLUSIONS: BZBS preserves testicular morphology and spermatogenesis possibly via inhibition of oxidative stress and the modulation of the Sirt6/P53 and Sirt6/NF-κB signaling pathways. The results shed light on the beneficial effect of BZBS on sperm quality and fertility in aging males.

Glycyrrhizic acid ameliorates sodium nitrite-induced lung and salivary gland toxicity: Impact on oxidative stress, inflammation and fibrosis.

Despite wide application of sodium nitrite (SN) as food additive, it exhibits considerable side effects on various body organs at high dose or chronic exposure. The aim of this study was to test whether Glycyrrhizic acid (GA) could ameliorate SN-induced toxicity in lung and submandibular salivary gland (SMG). A sample size of 30 adult male albino rats was randomly allocated into 3 groups. Group 1 served as control group. Rats were treated orally with 80 mg/kg of SN in group 2 or SN preceded by (15 mg/kg) GA in group 3. Lung & SMG tissues were used for oxidative stress assessment, examination of histopathological changes, fibrosis (MTC, TGF-ß and α-SMA) and inflammation (TNF-α, IL-1ß and CD-68). Concurrent administration of GA ameliorated pulmonary and salivary SN-induced toxicity via restoring the antioxidant defense mechanisms with reduction of MDA levels. GA reduced the key regulators of fibrosis TGF-ß and α-SMA and collagen deposition. In addition to reduction of inflammatory cytokine (TNF-α, IL-1ß) and macrophages recruitments, GA amended both pulmonary and salivary morphological changes. The present study proposed GA as a promising natural herb with antioxidant, anti-inflammatory and antifibrotic effects against pulmonary and salivary SN-induced toxicity.

Chlorella vulgaris ameliorates sodium nitrite-induced hepatotoxicity in rats.

The current was conducted to evaluate the ameliorating effect of Chlorella vulgaris (CV) extract against sodium nitrite-induced hepatotoxicity in rats. Forty-five rats were allocated randomly into 5 groups (n = 9). Group I (GI), control group: orally gavaged with normal saline daily. Group II (GII): orally gavaged with CV extract (70 mg/kg BW) for 3 months. Group III (GIII): orally gavaged with sodium nitrite (80 mg/kg BW) for 3 months. Group IV (GIV): received sodium nitrite as GIII and CV extract as GII simultaneously for 3 months. Group V (GV): received CV extract as GII and then, sodium nitrite as in GIII from the end of first month until the end of the experiment. Sodium nitrite significantly increased the activities of serum alanine aminotransferase, aspartate aminotransferase, and serum concentrations of tumor interleukin 1-ß and necrosis factor α. In addition, it increased concentrations of malondialdehyde and nitric oxide and expression level of caspase-3 in the hepatic tissue. However, it decreased activities of hepatic glutathione peroxidase, catalase, and superoxide dismutase and induced degenerative and necrotic changes in hepatic tissues. In contrast, CV extract administration modulated sodium nitrite-induced inflammation, oxidative stress, and alteration in hepatic tissue function and architecture. This study indicated that CV extract modulated sodium nitrite-induced hepatic toxicity through decreasing oxidative stress and inflammation and enhancing antioxidant enzyme activities in hepatic tissue of rats.

Mechanism underlying nephroprotective property of curcumin against sodium nitrite-induced nephrotoxicity in male Wistar rat.

The current work examined the outcome of curcumin (20 mg/kg body weight/day) administration on arginase and adenosine deaminase (ADA) activities and other kidney markers, as well as markers of oxidative stress, in Wistar rats exposed to sodium nitrite (NaNO2 ) (60 mg/kg of body weight, single dose) for 28 days. The results revealed that the NaNO2 exposed rats had significantly altered the ADA activities, arginase activities alongside other biomarkers of kidney function, and oxidative stress. However, pretreatment with curcumin significantly mitigated the altered activities ADA and arginase as well as other parameters. This was supported by the histopathological examination of the kidney tissues. Our findings suggest that the alteration in the activities of ADA and arginase could be involved in the mechanism of action employed by NaNO2 and curcumin in the respective induction and prevention of nephrotoxicity. PRACTICAL APPLICATIONS: These results suggest that moderate exposure to the acceptable daily dose of curcumin can improve food-related kidney damage through regulations of ADA and arginase activities, enhancement in the antioxidant system, and suppression of lipid peroxidation.

Sodium nitrite negatively affects reproductive ability and offspring survival in female mice.

Sodium nitrite (NaNO2) is an industrial chemical that is frequently used as a food additive to prevent botulism and enhance glossiness, such as curing meat. In addition, in some regions, water source NaNO2 concentrations exceed standard regulatory levels. Whether the excessive intake of NaNO2 has toxic effects on female fertility and fetal development remain unknown. In this study, we administered ICR mice control saline, low-dose NaNO2 (60 mg/kg/day), or high-dose NaNO2 (120 mg/kg/day) by intragastric gavage for 21 days. We then assessed oocyte morphology, spindle-chromosome dynamics, mitochondrial distribution, ATP content, apoptotic cell numbers, DNA damage levels, histone modifications, reactive oxygen species (ROS) levels, and offspring survival. Results showed that NaNO2 treatment decreased oocyte number, impaired polar body extrusion, and increased zona pellucida thickness in oocytes. Furthermore, NaNO2 disrupted MII spindle integrity, caused abnormal mitochondrial distribution, decreased ATP content, and increased levels of ROS and H3K4me2. Moreover, the number of oocytes in early stages of apoptosis and with levels of DNA damage increased in NaNO2-treated mice along with decreased offspring numbers and survival rates. We demonstrated the negative effects of NaNO2 on female reproductive abilities in mice.

Protective effect of carnosine and N-acetylcysteine against sodium nitrite-induced oxidative stress and DNA damage in rat intestine.

The widespread use of sodium nitrite (NaNO2) as food preservative, rampant use of nitrogenous fertilizers for agricultural practices, and improper disposal of nitrogenous wastes have drastically increased human exposure to high nitrite levels causing various health disorders and death. In the present study, the protective effect of carnosine and N-acetylcysteine (NAC) against NaNO2-induced intestinal toxicity in rats was investigated. Animals were given a single acute oral dose of NaNO2 at 60 mg/kg body weight with or without prior administration of either carnosine at 100 mg/kg body weight/day for 7 days or NAC at 100 mg/kg body weight/day for 5 days. Rats were killed after 24 h, and intestinal preparations were used for the evaluation of biochemical alterations and histological abrasions. Administration of NaNO2 alone decreased the activities of intestinal brush border membrane and metabolic enzymes and significantly weakened the anti-oxidant defense system. DNA damage was also evident as observed by increased DNA-protein crosslinking and fragmentation. However, prior administration of carnosine or NAC significantly ameliorated NaNO2-induced damage in intestinal cells. Histological studies support these biochemical results, showing intestinal damage in NaNO2-treated animals and reduced tissue injury in the combination groups. The intrinsic anti-oxidant properties of carnosine and NAC must have contributed to the observed mitigation of nitrite-induced metabolic alterations and oxidative damage. Based on further validation from clinical trials, carnosine and NAC can potentially be used as chemo-preventive agents against NaNO2 toxicity.

Carnosine and N-acetyl cysteine protect against sodium nitrite-induced oxidative stress in rat blood.

Sodium nitrite (NaNO2 ) is widely used in the food industry as a preservative and colorant in meat and fish products. Industrialization and improper agricultural practices have greatly increased human exposure to high nitrite levels, mainly through contaminated drinking water, causing various health disorders. We have investigated the protective effect of carnosine (CAR) and N-acetyl cysteine (NAC) on NaNO2 -induced toxicity in rat blood. CAR is a bioactive dipeptide found in mammalian muscle while NAC is a synthetic sulfhydryl amino acid and an important precursor of glutathione. Animals were given a single acute oral dose of NaNO2 at 60 mg/kg body weight with or without prior administration of either CAR or NAC. Rats were sacrificed after 24 h, blood was withdrawn and plasma and erythrocytes were isolated. Administration of NaNO2 alone increased methemoglobin levels and methemoglobin reductase activity, decreased the activities of antioxidant defense and metabolic enzymes and significantly weakened the total antioxidant capacity of rat erythrocytes. Similar effects were seen in plasma of NaNO2 -treated rats. In contrast, administration of CAR or NAC, prior to NaNO2 treatment, markedly attenuated the NaNO2 -elicited deleterious effects. Thus, CAR and NAC can mitigate nitrite-induced metabolic alterations and oxidative damage probably due to their intrinsic biochemical antioxidant properties. This study suggests that CAR and NAC can be potentially used as therapeutic/protective agents against NaNO2 toxicity.

In vivo-like 3-D model for sodium nitrite- and acrylamide-induced hepatotoxicity tests utilizing HepG2 cells entrapped in micro-hollow fibers.

To address the need for a high throughput toxicity test in the modern food industry, an in vivo-like 3-D cell model was constructed in this study to provide an alternative to controversial long-term animal models and to improve the sensitivity and accuracy of the traditional monolayer model. The model formed cell cylindroids within polyvinylidene fluoride (PVDF) hollow fibers and therefore mimicked the microenvironment of liver tissue. Microscopy methods were used, and liver-specific functions were measured to demonstrate the superiority of the model compared to the monolayer model, as well as to optimize the model for best cell performances. Later, toxicity tests of sodium nitrite and acrylamide were conducted in both the 3-D model and the monolayer model to study the sensitivity of the 3-D model in toxicity responses. As expected, HepG2 cells within the 3-D model responded at lower concentrations and shorter exposure times compared to cells within the monolayer model. Furthermore, western blot analysis of apoptosis pathways also supported the argument.

Downregulation of HIF1-α, Smad-2, AKT, and Bax gene expression in sodium nitrite-induced lung injury via some antioxidants.

The aim of the current study is to evaluate the efficacy of pretreatment with either l-arginine (L-arg) or Carnosine (Car) and their combination in ameliorating some of the biochemical indices induced in the lung of sodium nitrite (NaNO2 )-intoxicated rats. The results revealed that NaNO2 significantly increased serum tumor necrosis factor-α, C-reactive protein, heat shock proteins-70, vascular endothelial growth factor, and Interleukin 6. Moreover, transforming growth factor-ß, hypoxia-inducible factor, Smad-2, Protein Kinase B (AKT), and Bax were overexpressed, whereas Bcl2 protein was downregulated compared with the normoxic group. The administration of the fore mentioned antioxidants, either alone or in combination, markedly downregulated the previously mentioned inflammatory, apoptotic, as well as the fibrotic markers in lung tissue compared with the NaNO2 -intoxicated rats. The histopathological examination reinforced the previous results. In conclusion, the current data revealed the efficacy of l-arg and Car in ameliorating the pulmonary damage via suppression of the inflammatory markers in response to NaNO2 -intoxication. Interestingly the combination regimen showed the most significant effect.

Quercetin inhibits sodium nitrite-induced inflammation and apoptosis in different rats organs by suppressing Bax, HIF1-α, TGF-ß, Smad-2, and AKT pathways.

The objective of this work is to study the protective effects of Quercetin against sodium nitrite-induced hypoxia on liver, lung, kidney and cardiac tissues, also to explore novel mechanism of this compound. Male albino rats were injected with sodium nitrite (75 mg/kg). Quercetin (200 mg kg-1 ,- i.p.) was administrated 24 and 1 h respectively prior to sodium nitrite intoxication, hypoxia significantly decreased hemoglobin concentration, while increased expressions of HIF, Bax, Smad-2, TGF-ß, and AKT. However, administration of Quercetin played a modulatory role against the previous mentioned apoptotic factors protein expressions in all the studied tissues. On the other hand, Bcl-2 was downregulated by NaNO2 , whereas concurrent treatment with Quercetin increased its expression. It was concluded that Quercetin possesses an anti-apoptotic action induced by NaNO2 -intoxication via different mechanisms. Quercetin administration is recommended in areas of high altitudes to combat the hazard effect of hypoxia in different organs and in some diseases accompanied by hypoxic stress.

Suggestive evidence for the induction of colonic aberrant crypts in mice fed sodium nitrite.

A reported linkage between processed (nitrite-treated) meat products and the incidence of colon cancer could be due to sodium nitrite (NaNO2) itself or to N-nitroso compounds produced from the nitrite. Exposure to nitrite occurs due to residual nitrite in processed meat and to salivary nitrite arising by reduction of nitrate in vegetables and drinking water. Here we tested whether NaNO2 could induce colonic aberrant crypts (ABC) or ABC foci (ACF), which are putative precursors of colon cancer. We fed NaNO2 in drinking water for 20-25 wk to groups of 8-20 adult female mice. After sacrifice, ABC and ACF were counted in 2-cm distal colonic segments. In Experiment 1, no significant differences in ABC/ACF induction were seen between groups of 13-14 A/J mice fed 0, 0.5, or 1.0 g NaNO2/l drinking water. NaNO2 also did not affect fasting blood glucose levels. In Experiment 2, we fed 0, 1.0, 1.25, or 1.5 g NaNO2/l water to groups of 15 CF-1 mice. Five of the mice fed 1.5 g NaNO2/l showed ABC, whereas all other groups showed only 0-2 ABC/group, including 0 ABC for the group fed 1.25 g NaNO2/l. Overall statistical analysis indicated a dose-response p trends of 0.04. Pairwise comparison of ABC between groups fed 1.25 and 1.5 g NaNO2/l showed p 0.02 for both ABC and ACF, but a similar comparison between the untreated and 1.5 g/l groups showed no significant effects. In Experiment 3, hot dogs (18% of diet), which were fed to CF-1 mice previously treated with azoxymethane, inhibited ABC and ACF induction, but this effect was not significant (P = 0.10-0.12). In conclusion, these results support the view that NaNO2 may be a risk factor for colon carcinogenesis.

Thymoquinone ameliorates testicular tissue inflammation induced by chronic administration of oral sodium nitrite.

Although sodium nitrite has been widely used as food preservative, building bases of scientific evidence about nitrite continues to oppose the general safety in human health. Moreover, thymoquinone (TQ) has therapeutic potential as antioxidant, anti-inflammatory, antibacterial and anticancer. Therefore, we investigated the effects of both sodium nitrite and TQ on testicular tissues of rats. Forty adult male Sprague Dawley rats were used. They received either 80 mg kg(-1) sodium nitrite or 50 mg kg(-1) TQ daily for twelve weeks. Serum testosterone was measured. Testis were weighed and the testicular tissue homogenates were used for measurements of tumour necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-4, IL-6, IL10, caspase-3, caspase-8 and caspase-9. Sodium nitrite resulted in significant reduction in serum testosterone concentration and elevation in testis weight and Gonado-Somatic Index. We found significant reduction in testicular tissues levels of IL-4 and IL-10 associated with elevated levels of TNF-α, IL-1ß, IL-6, caspase-3, caspase-8 and caspase-9. In conclusion, chronic oral sodium nitrite induced changes in the weight of rat testis accompanied by elevation in the testicular tissue level of oxidative stress markers and inflammatory cytokines. TQ attenuated sodium nitrite-induced testicular tissue damage through blocking oxidative stress, restoration of normal inflammatory cytokines balance and blocking of apoptosis.

Nigella sativa oil attenuates chronic nephrotoxicity induced by oral sodium nitrite: Effects on tissue fibrosis and apoptosis.

OBJECTIVES: Sodium nitrite, a food preservative, has been reported to increase oxidative stress indicators such as lipid peroxidation, which can affect different organs including the kidney. Here, we investigated the toxic effects of oral sodium nitrite on kidney function in rats and evaluated potential protective effects of Nigella sativa oil (NSO). METHODS: Seventy adult male Sprague-Dawley rats received 80 mg/kg sodium nitrite orally in the presence or absence of NSO (2.5, 5, and 10 ml/kg) for 12 weeks. Morphological changes were assessed by hematoxylin and eosin, Mallory trichome, and periodic acid-Schiff staining. Renal tissues were used for measurements of oxidative stress markers, C-reactive protein, cytochrome C oxidase, transforming growth factor (TGF)-beta1, monocyte chemotactic protein (MCP)-1, pJNK/JNK, and caspase-3. RESULTS: NSO significantly reduced sodium nitrite-induced elevation in serum urea and creatinine, as well as increasing normal appearance of renal tissue. NSO also prevented reductions in glycogen levels caused by sodium nitrite alone. Moreover, NSO treatment resulted in dose-dependent significant reductions in fibrosis markers after sodium nitrite-induced 3- and 2.7-fold increase in MCP-1 and TGF-beta1, respectively. Finally, NSO partially reduced the elevated caspase-3 and pJNK/JNK. DISCUSSION: NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.

Sodium nitrite-induced oxidative stress causes membrane damage, protein oxidation, lipid peroxidation and alters major metabolic pathways in human erythrocytes.

Nitrite salts are present as contaminants in drinking water and in the food and feed chain. In this work, the effect of sodium nitrite (NaNO2) on human erythrocytes was studied under in vitro conditions. Incubation of erythrocytes with 0.1-10.0 mM NaNO2 at 37 °C for 30 min resulted in dose dependent decrease in the levels of reduced glutathione, total sulfhydryl and amino groups. It was accompanied by increase in hemoglobin oxidation and aggregation, lipid peroxidation, protein oxidation and hydrogen peroxide levels suggesting the induction of oxidative stress. Activities of all major erythrocyte antioxidant defense enzymes were decreased in NaNO2-treated erythrocytes. The activities of enzymes of glycolytic and pentose phosphate pathways were also compromised. However, there was a significant increase in acid phosphatase and also AMP deaminase, a marker of erythrocyte oxidative stress. Thus, the major metabolic pathways of cell were altered. Erythrocyte membrane damage was suggested by lowered activities of membrane bound enzymes and confirmed by electron microscopic images. These results show that NaNO2-induced oxidative stress causes hemoglobin denaturation and aggregation, weakens the cellular antioxidant defense mechanism, damages the cell membrane and also perturbs normal energy metabolism in erythrocytes. This nitrite-induced damage can reduce erythrocyte life span in the blood.

Chosen quality parameters of pork sausage produced without curing mixture.

BACKGROUND: The aim of this study was to determine the influence of the dried celeriac juice addition, as a nitrogenous compounds sources, on the quality of the experimental pork sausage. METHODS: In the sausages with vegetable preparation addition and in traditionally cured sausages amount of the sodium nitrate (III) and sodium nitrate (V) was determined (in the batter and 24 h after production). Moreover the total number of aerobic bacteria, number of coli forms, anaerobic survived bacteria, coagulase positive staphylococci, Listeria monocytogenes and occurrence of Salmonella in 25 g (according to Polish Standards) was determined during sausages storing (after 2, 14 and 21 days). Also sensory evaluation was carried out (after 2 and 14 days). After 2, 7, 14 and 21 days the amount of drip loss in the package was determined. Result. In the experimental sausage produced with the addition of vegetable preparation (E0), the content was 2.2 times higher of sodium nitrate (V) while sodium nitrate (III) three times lower, compared to traditionally cured sausages (K). In the E0 sausages faster aerobic microorganisms proliferation was observed. However, in these products, in comparison to the control group (K), no higher contamination with coliform bacteria, anaerobic sporulating bacteria, coagulase positive Staphylococci, Listeria monocytogenes or Salmonella was found. The sensory evaluation (colour in cross-section, flavour, taste, consistency) showed no statistically significant difference between the experimental sausages. Conclusions. In the sausages produced with dried celeriac juice addition there was above twice more sodium nitrate (V) and threefold less sodium nitrate (III) in comparison to traditionally cured sausages and faster growth of aerobic bacteria was demonstrated. Sensory quality of 'cold' and 'hot' sausages without curing salt was worse, but the score num. RESULTS: nd. The aim of this study was to determine the influence of the dried celeriac juice addition, as a nitrogenous compounds sources, on the quality of the experimental pork sausage. Material and methods. In the sausages with vegetable preparation addition and in traditionally cured sausages amount of the sodium nitrate (III) and sodium nitrate (V) was determined (in the batter and 24 h after production). Moreover the total number of aerobic bacteria, number of coli forms, anaerobic survived bacteria, coagulase positive staphylococci, Listeria monocytogenes and occurrence of Salmonella in 25 g (according to Polish Standards) was determined during sausages storing (after 2, 14 and 21 days). Also sensory evaluation was carried out (after 2 and 14 days). After 2, 7, 14 and 21 days the amount of drip loss in the package was determined. Result. In the experimental sausage produced with the addition of vegetable preparation (E0), the content was 2.2 times higher of sodium nitrate (V) while sodium nitrate (III) three times lower, compared to traditionally cured sausages (K). In the E0 sausages faster aerobic microorganisms proliferation was observed. However, in these products, in comparison to the control group (K), no higher contamination with coliform bacteria, anaerobic sporulating bacteria, coagulase positive Staphylococci, Listeria monocytogenes or Salmonella was found. The sensory evaluation (colour in cross-section, flavour, taste, consistency) showed no statistically significant difference between the experimental sausages. CONCLUSIONS: In the sausages produced with dried celeriac juice addition there was above twice more sodium nitrate (V) and threefold less sodium nitrate (III) in comparison to traditionally cured sausages and faster growth of aerobic bacteria was demonstrated. Sensory quality of 'cold' and 'hot' sausages without curing salt was worse, but the score number was never lower than 4,1, so the sausages were accepted. In the vacuum packaged sausages produced with the addition of vegetable preparation higher, about 0.3-0.4 percent score, drip loss was found.

Urinary excretion of N-nitroso compounds in rats fed sodium nitrite and/or hot dogs.

Nitrite-treated meat is a reported risk factor for colon cancer. Mice that ingested sodium nitrite (NaNO2) or hot dogs (a nitrite-treated product) showed increased fecal excretion of apparent N-nitroso compounds (ANC). Here, we investigated for the first time whether rats excrete increased amounts of ANC in their urine after they are fed NaNO2 and/or hot dogs. Rats were treated for 7 days with NaNO2 in drinking water or were fed hot dogs. Their 24 h urine samples were analyzed for ANC by thermal energy analysis on days 1-4 after nitrite or hot dog treatment was stopped. For two rats fed 480 mg NaNO2/L drinking water, mean urinary ANC excretion on days 1-4 was 30, 5.2, 2.5, and 0.8 nmol/day, respectively. For two to eight rats/dose given varied NaNO2 doses, mean urinary ANC output on day 1 increased from 0.9 (for no nitrite) to 37 (for 1000 mg NaNO2/L drinking water) nmol ANC/day. Urine samples of four rats fed 40-60% hot dogs contained 12-13 nmol ANC on day 1. Linear regression analysis showed highly significant correlations between urinary ANC excretion on day 1 after stopping treatment and varied (a) NaNO2 level in drinking water for rats fed semipurified or commercials diet and (b) hot dog levels in the diet. Some correlations remained significant up to 4 days after nitrite treatment was stopped. Urinary output of ANC precursors (compounds that yield ANC after mild nitrosation) for rats fed semipurified or commercial diet was 11-17 or 23-48 µmol/day, respectively. Nitrosothiols and iron nitrosyls were not detected in urinary ANC and ANCP. Excretion of urinary ANC was about 60% of fecal ANC excretion for 1 to 2 days after NaNO2 was fed. Administered NaNO2 was not excreted unchanged in rat urine. We conclude that urinary ANC excretion in humans could usefully be surveyed to indicate exposure to N-nitroso compounds.