Sodium Nitrite and Oxidative Stress

The following sample essay on “Sodium Nitrite and Oxidative Stress”: definition of Sodium Nitrite and oxidative stress on health.

NaNO2 is an inorganic yellowish white crystal compound composed of sodium,nitrogen and oxygen atoms with a total of molecular weight of 68.995g/mol.It is a basic compound with a pH of 9 with melting and boiling point of 271OC and 320OC respectively(A.Young, 2008) and it is highly soluble in water (Parthasarathy & Bryan, 2012).

NaNO2 replaced the old ways of preserving meet and poultry products such as the use of potasium nitrate (KNO3) and use of smokes to control spoilage of food and maximize the shelf-life.

This made the cured meat and poultry products with a unique special flavor and made the products to be available during scacity. NaNO2 made the products to be with attractive colour texture and teste that can not be substituted by other preserving compound and therefore the quality of the products preserved with NaNO2 can be easily distinguished with other products used different preservation materials.

Apart from increasing the quality and extending the storage period of meat and poutry products NaNO2 from vegitables has reported to have healthy advantages including control blood pressure, immune system, wound repair, neurological functions, control blood flow in cardiac muscles and preventing various cardiovascular diseases such as hypertention, alterosclerosis and stroke. Furthermore Hord et al., (2009) reported that even the vascular system have a potential of production of endogeneous nitrites and NO which serve the same purpose as explained by Sindelar & Milkowski (2011).

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About 70% of the vasculature endogensous NO is produced by the enzymes known as endothelia nitric oxide synthesase(eNOS) which produce NO from amino acid L-arginine and molecular oxygen (Hord et al., 2009).

Despite of its amazing advantages, NaNO2 left with no controvasial on its uses.This is due to the reaction of the compound with amines and amides to produce carcinogenic compounds known as nitrosyl and nitroso compounds. The compounds are dangerous to the health of human since are associated with cancer and leukemia and chronic exposure to the compound can cause inflamation and apoptosis of various cells in several tissues(Alyoussef & Al-gayyar, 2016). The same idea was reported by Hassan et al.,(2009) who stated that NaNO2 cause hepatotoxicity, methaemoglobenemia, tissue injury, impared inflamatory responses, stunted growth and hormone problems. It was accepted that although NaNO2 can cause cancer is a weak carcinogenic compound especillly at the squamous epithelium of the forestomach.It was found that exposing wistar rate to 0.3% NaNO2 for 12 months caused squamous papillomas at the forestomach. Furthermore exposing the same concentration of NaNO2 to F344 rats via drinking water for 28 weeks amplified the prevalence of forestomach neoplasm in the post-initiation period(Hassan et al., 2009).

NaNO2 can change the colur of meat to red or shaded pink that are liked my many consumers. For the process of changing the colour of the meat only small amount of NaNO2 of about 2-14 part per milion(ppm) is needed, however to rise the shelf-life of preserved and to prevent fading and non uniform curing of meat a high amount of NaNO2 is needed of about 25-50 ppm(Salama et al., 2013). Although small amount of NaNO2 is needed for color change, a large amount of the compound of about 156 ppm is needed for production of the best color, flavour and for extended long shlf-life(Sindelar & Milkowski, 2011).

Sodium nitrite’s lethal dose LD50 in rats is 180 mg/kg and its human LD50 is 71 mg/kg(Salama et al., 2013). This is to say the approximately LD50 in adults human is 2.6g however there is a case reported a patient survived afterconsuming 6g of sodium nitrite(Katabami, Hayakawa, & Gando, 2016).After added to the meat NaNO2 will combine or react with various chemicals substance including protein, then the concentration of NaNO2 will decrease per time until reaches an undetectable concentration called residure nitrite(10-15ppm) that principlally will maintain the shelf life of cured meat and poultry.

The formation of colour depends on the convension of NaNO2 to NO which then reacts with myglobin to form nitrosylating agent which produce the red colour of cured meat.The idea agreed by Parthasarathy & Bryan (2012) who explained that nitrite combines with hemoglobin to form nitrosylhemoglobin, which later gets converted to nitrosylhemochromogen when heated.The naturally occurring myoglobin reacts with the nitrite compounds, to form nitrosylmyoglobin which is bright red in color, and an axial ligand NO is coordinated to the central heme iron. The process can be affected by various factors including pH,meat system,amount of reductants available,temperature and time of exposure (Sindelar & Milkowski, 2011) .The same reaction can occurs when nitrite is consumed by human.Salama et al.,(2013) explained that the reaction takes place in the human stomach where nitrite reacts with secondary amines under acidic condition.

Nitrite reduction to nitric oxide can be carried out by numerous metalloproteins, enzymes, and compounds with redox potential, comprising of hemoglobin, deoxyhemoglobin, deoxymyoglobin, xanthine oxidoreductase, ascorbic acid, and polyphenols. The process of reduction significantly heightened during the stress of hypoxemia and ischemia(Hord et al., 2009).

NaNO2 found to have antioxidantat and antimicrobial properties.The properties thought to come from its ability to bind with heme (myoglobin and hemoglobin) protein and metal ions and chellating free radicals. 200ppm of NaNO2 found to cause 12-fold decrease of thiobarbituric acid (TBA)(Sindelar & Milkowski, 2011), on other hand the increase of thiobarbituric acid reactive substances (TBARS) indicating the effects of lipid peroxidation initiated by the peroxidation of poly-unsaturated fatty acids (PUFA) of cell lipoprotein, phospholipids and cholesterol ester (Ahmad, Yousaf, Wahab, & Kamran, 2018; Anwar & Mohamed, 2014) in the liver by addition of nitrosamine precasor (Hassan & Yousef, 2010). Also the the same ppm of 200 prevented the growth Staphylococcus aureus, Salmonella and only 0.6% of NaNO2 in meat is enough to prevent the growth of Clostridium botulinum spores by its ability to prevents of iron-sulfur groups which are very important in energy production (Alyoussef & Al-gayyar, 2016;Salama et al., 2013).

Figure 1:Change in colour of meat cured with Sodium Nitrite (Parthasarathy & Bryan, 2012)

Oxidative stress

Oxidative stress occurs either when there are more oxidants than antioxidants in the defense system or when there is depleted antioxidant. Many oxidants are oxygen and nitrogen species although there are other oxidants that are not either oxygen or nitrogen species such as hypochlorous acid. Several liver diseases and disorders such as hepatitis, fibrosis, cirrhosis, autoimmune liver diseases, alcohol liver diseases and hepatocellular carcinoma are the results of oxidative stress. The effects of ROS and RNS depends on their ability of interact with all cellular macromolecules resulting into cleaving the phosphodiester bonds holding bases in RNA and DNA together, breaking the chain structure of RNA and DNA(Muriel & Gordillo, 2016).

Generally oxidative stress caused by oxidants cause effects in five common ways. Firstly, oxidants cause generation of modified biomolecules leads to abnormal cellular function. Secondly, the oxidants can lead to the formation of other toxic substances such as peroxides, alcohol, aldehydes and ketones. Thirdly, they can initiate autoimmune response by changing several biomolecules. The fourth way in which oxidants promote cellular destruction is by modifying signaling cascades which may results in amplifying their effects. The signaling cascades that can be modified by oxidants are stress-activated protein kinase, intracellular calcium, transcription factors (activator protein-1, hypoxia inducible factor-1, nuclear factor-?B (NF-?B)), and modulators of apoptosis signaling. Finally, oxidants can influence intercellular signaling via activation of cytokine expressions. For example, oxidant-induced activation of NF-?B in Kupffer cells stimulates production of proinflammatory tumor necrosis factor (TNF)-? by these cells(Moreno-otero, 2005).

After converted to NO by various mechanisms, the NO form methemoglobin in the blood from its reaction with hemoglobin which is responsible for carrying oxygen and transport it in the circulation system. This cause hypoxia because the affinity of methemoglobin to oxygen is less than the capacity of hemoglobin. This is due to the NO which reduce the ferrous ion into ferric ion. Hypoxia increases the chance of formation of oxidative stress by stimulates the mitochondria to bust and generate ROS and protein carboxylation in response to deficiency of oxygen induce oxidative stress affecting specific protein.

ROS and RNS are produced in mitochondria only, but in many organelles and structures in the cell such as endoplasmic reticulum, cytosol, microsomes, lysosomes, peroxisomes, neutrophils and macrophage during various metabolic pathways (figure 3). The main site of ROS and RNS production within the cells is the mitochondrial electron transport system including complex I (NADH-Ubiquinone oxidoreductase) and complex II (Cytochrome C-Oxidase)(Mello et al., 2016). In the presence of oxidase or xanthinoxidase the oxygen molecules that are not used in respiration are converted to ROS peroxide. Superoxide is the main starting point of oxidative stress by meaning that it results in production of other oxidants through various processes and reactions (Figure 2). The superoxide can be converted into another ROS sodium peroxide by SOD. In the Fenton reaction sodium peroxide can be converted to another ROS hydroxyl radical and water. In the presence of myeloperoxidase hydrogen peroxide can be converted to another oxidant hypochlorous acid. With the availability of CAT or GSH-peroxidase, the sodium peroxide can be converted into water(Mello et al., 2016).

Figure 2: Mechanism of ROS and RNS formation in the Mitochondria (Moreno-otero, 2005)

In the liver RNS especially NO. are produced NOS. There are several NOS including Neuronal NOS, endothelial NOS of liver endothelia cells and inducible NOS (iNOS) of hepatocytes, Kupffer cells, cholangiocytes and non-parenchymal cells such as Stellate cells. The level of oxidative stress and cytokine control the iNOS. Inflammation caused by cytokine-activated neutrophil or lymphocytes also produce NO• in the liver. Apart from NO., peroxynitrite is another RNS that can be produced in the liver cells. It is produced when superoxide can react with NO. The reverse reaction of peroxynitrite with glutathione can produce NO• radicals. RNS specifically NO. have beneficial and detrimental impacts in the liver(Hord et al., 2009). The beneficial impacts are; it acts as vasodilator factor to maintain passage of blood through circulatory system to the tissue bed and prevent blood clot formation. NO. is an antiapoptotic in the liver inflammation to prevent programmed cell death. As an antioxidant NO. can stop a chain reaction initiated by other oxidants by scavenging lipid peroxides radicals. Another positive effect of NO. is based on its necessity in live regeneration. In other hand the detrimental impacts of NO. include formation of nitro tyrosine which cause cellular disfunction and necrosis. In addition to that NO. can cause DNA damage by depleting the cellular pyridine nucleotide resulting into impaired cellular functions (AT?LA USLU, G., USLU, H., & ADALI, 2019).

Figure 3: Sources of ROS and RNS in the Cell (Mello et al., 2016)