A preservative is any material able to prevent, slow down, or stop the growth of microorganisms, as well as any food deterioration caused by microorganisms. Preservatives can be antimicrobial, inhibiting the growth of bacteria or fungi, or antioxidants, which operate similarly to oxygen absorbers by inhibiting the oxidation of food constituents. Traditional preservatives also include natural compounds such as sugar, ginger, alcohol, and diatomaceous earth. Calcium propionate, sodium nitrate, sodium benzoate, sodium nitrite, sulfites (sulphur dioxide, sodium bisulfite, potassium hydrogen sulfite, etc.), and disodium are examples of common chemical preservatives [8]. The preservatives that cause teratogenicity are noted below.
Sodium benzoate ( ) is a synthetic food preservative, which is extensively used in food, medicinal, and cosmetics diligence. The chemical is a sodium salt of benzoic acid that is safe to eat and apply to the skin. It should not be used in some acidic products because it can interact with other chemicals to induce dangerous composites, but it is not poisonous or irritable to tissue. It dissolves easily in water, and its inclusion in food is approved as it is able to prevent the growth of molds and other microbes. The negative effects of sodium benzoate on health have been established, including cellular damage. Numerous research has been conducted in recent years on the use of natural elements with various purposes in food, with some success, but there is still a need to study in the food sector. The teratogenic impact of sodium benzoate is discussed below with the assistance of a study of fetal deformations due to long-term consumption of sodium benzoate in pregnant BALB/c mice [9].
Open in a separate window(1) Mechanism of Action. A high dosage of sodium benzoate can induce histamine to be released from the body. H1 receptors are affected by mast cell granules and histamine accessible in endothelial cells, leading to a rise in artery diameter leaking of elements of blood plasma and its permeability in the tissues. As a result, it is suitable to assign hemorrhages, and physical tissue damage reported in sodium benzoate affects the skin of embryos by this way. Sodium benzoate enters into blood vessels and interfere with genes, which is invloeved in the synthesis of blood clotting factors [10]. The studies have also shown the cytogenetic goods of benzoic acid sodium salts in lymphocytes [11]. In mice, exposure to methylnitrosourea (MNU) caused proliferating cell damage via macromolecule alkylation and the production of reactive oxygen species (ROS). Elevated ROS levels in mice lowered the severity of retinal abnormalities and, though unknown mechanisms, inhibited fetal Pax-3 gene expression, which is crucial in neural tube development blockage [12]. In proliferating embryonic tissues of rats, increased ROS suppresses the expression of the bcl-2 (antiapoptotic) gene. Rajadurai and Prince (2006) have reported that elevated production of ROS in the biological system showed adverse effects on nuclei acids [13].
Some benzoate derivations, such as SB, appear to be free radical scavengers in humans [14], whereas other mechanisms possibly causing embryonic hemorrhage and eye tissue disorders after PB exposure may result from the induction of potentially harmful ROS situations in embryonic tissues (such as the eye) and inhibit embryonic gene expression, such as Pax-3 or alternative genes required for blood clotting. Our study's findings are related to hyperkalemia, which has been associated to intraventricular hemorrhage in premature neonates. Researchers hypothesized that low systemic blood flow, as measured by lower urine output and K+ secretion, could contribute to the development of hyperkalemia in premature neonates [15]. It is also believed that the hemolytic activity of the limited intraventricular blood clot contributes to an intraventricular K+ load surplus [16].
(2) Adverse Effects. The current study's findings on the teratogenic effects of sodium benzoate on embryo revealed a variety of defects, including craniofacial deformities. Mandibular hypoplasia and other forms of mandibular hypoplasia are the most common calvarias deformity and vertebral column deformation. Scoliosis and neural tube defects (NTDs) are two examples of this. It had been argued in a study that administering high doses of antibiotics on a daily basis sodium benzoate has the potential to be genotoxic and teratogenic modifications in the neurological system [17]. The other severe impacts also include on growth factors, cell cycle, and gene expression, as well as the fact that it can cause deformations during birth. Food additives in general must be reevaluated as needed in light of new information shifting usage situations and fresh scientific findings information.
Potassium benzoate ( ) is an odorless white powder made by heating benzoic acid and potassium salt together. Benzoic acid is a naturally occurring chemical found in plants, animals, and fermented foods. It was once made from the benzoin resin of particular tree species, but it is now largely made in factories. Salt beds or minerals are the most common sources of potassium salts. PB is used as a preservative because it prevents bacteria, yeast, and mold from growing. As a result, it is frequently used to increase the shelf life of food, beauty, and skin care goods. The teratogenicity of potassium benzoate is defined by an experiment “Teratogenic Effects of Long-term Consumption of Potassium Benzoate on Eye Development in BALB/c Fetal Mice” [18].
Open in a separate window(1) Mechanism of Action. It has also been observed that potassium benzoate suppresses intracellular protein and DNA synthesis at doses below 100 pg/ml and over 500 pg/ml. The study found that benzoic acid (200 and 500 pg/ml) increases chromosomal abnormalities, sister chromatid exchanges, and micronucleus prevalence in human cells without changing the medium pH [19]. There is some suggestion that a mutation in the homeobox gene, OTX2, may also be implicated in the development of these symptoms. The expression pattern of the OTX2 gene in human embryo is also linked to bilateral anophthalmia to certain retinal consequences and pigmentary retinopathy [20]. Because PB can be mutagenic, various studies have been done to precisely investigate the potential teratogenic effects of the food preservative, PB, on the embryonic eye development in pregnant mice. The findings showed that pregnant mice exposed to PB experienced severe bleeding of the embryonic eye, a malformed lens, and retinal folds with underdeveloped layers. Because of the complexity of eye development, many congenital anomalies occur, but most of them are not common [21].
Congenital eye abnormalities can be caused by a variety of environmental teratogens. Some studies have found a link between the use of some antiepileptic medicines during pregnancy and congenital eye malformations such as anophthalmia, microphthalmia, or coloboma of the iris or optic disc [22]. Defects in the PAX6 gene expression cause aniridia-like iris abnormalities [23], corneal opacities, and lens-corneal adhesions similar to Peters' anomaly [24]. Detailed histologic examinations of neonatal mice with Peters-like abnormalities indicated that the lens commonly fails to detach from the cornea [25]. Furthermore, the study found that OTX2 loss-of-function mutations are linked to a wide range of ocular phenotypes, from bilateral anophthalmia to mild microphthalmia with retinal abnormalities [26].
Alqahtani et al. have investigated the cytogenetic effects of potassium salts of 1-p-(3-methyltriazeno) benzoic acid in human lymphocytes [7]. There was also a dose-dependent increase in chromosome breakage in human cells after exposure to 1-p-(3-methyltriazeno) benzoic acid potassium salts [27]. Dose-dependent administration of toxicant showed increased toxicity and reaches the saturation level at certain doses. As a result, PB and reduced cell proliferation, as well as PAX6 and OTX2 mutation, delayed normal eye development.
(2) Adverse Effect. The potential teratogenic effects of PB on embryonic eye development were investigated in the study. As a result of the exposure of pregnant mice to PB, severe bleeding of the embryonic eye, malformed lenses, and retinal folds with underdeveloped layers were observed. Many congenital defects occur as a result of the intricacy of eye development; however, the majority of them are uncommon [28]. Congenital eye abnormalities can be caused by a variety of environmental teratogens. Some researchers have discovered clear evidence of a link between antiepileptic drug use during pregnancy and congenital eye malformations including anophthalmia and microphthalmia [29].
Mice treated to methyl nitrosourea (MNU) during pregnancy suffered harm to proliferating cells due to macromolecule alkylation and reactive oxygen generation. Increased ROS in mice reduced the severity of retinal problems and blocked fetal Pax-3 gene expression, which is important for neural tube development, through unknown processes [30]. Other mechanisms that may cause embryonic bleeding and eye tissue abnormalities after PB exposure include the generation of potentially harmful ROS levels in embryonic tissues (such as the eye) and the inhibition of embryonic gene expression such as Pax-3 or alternative blood clotting genes. The above findings are comparable to those of hyperkalemia, which has been linked to intraventricular hemorrhage in premature babies. In our research, we discovered that PB-exposed mouse fetuses have significantly reduced weight and crown-rump lengths. Adult mice subjected to 280 and 560 mg/kg/day of PB for 20 days showed no adverse effects. As a result, it is thought that mouse embryos are more vulnerable to PB than adults. The above findings imply that PB has teratogenic effects on mouse fetuses' ocular development. Thus, further detailed investigations on its specific and general impacts are required [31].
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