Protective effects of Urtica dioica on the cerebral cortex damage induced by Potassium bromate in adult male albino rats.

Potassium bromate is used in cheese production, beer making and is also used in pharmaceutical and cosmetic. It is a proven carcinogen as it is a strong oxidizing agent that generates free radicals during xenobiotic metabolism. Urtica dioica (Ud) (from the plants' family of Urticaceae) is a plant that has long been used as a medicinal plant in many parts of the world. It has been shown to have anti-inflammatory, antioxidant and immunosuppressive properties. So, this study aimed to clarify the effect of Potassium bromate on the histological structure of cerebral cortex of adult male albino rats, evaluate the possible protective role of Urtica dioica. Thirty adult healthy male albino rats were divided into three groups; group I (Control group), group II (KBrO3 treated group). Group III (KBrO3 and Urtica dioica treated group).At the end of the experiment, rats in all groups were anesthetized and specimens were processed for light and electron microscope. Morphometric and statistical analyses were also performed. Nerve cells of the treated group showed irregular contours, dark nuclei, irregular nuclear envelopes, dilated RER cisternae, and mitochondria with ruptured cristae. Vacuolated neuropil was also observed. Immunohistochemically, stained sections for GFAP showed strong positive reaction in the processes of astrocytes. Recovery group showed revealed nearly the same as the histological picture as the control group. In conclusion, potassium bromate induces degenerative effects on neurons of cerebral cortex and urtica dioica provide an important neuroprotective effects against these damaging impacts through their antioxidant properties.

History, mechanism of action, and toxicity: a review of commonly used dough rheology improvers.

Dough rheology improvers, which often are oxidative reagents in nature, have long been used in bread-making industry to enhance protein crosslinking and subsequently improve the dough rheological properties and bread qualities. Numerous studies were conducted to explore the effects of these oxidative agents on dough quality improving, however, the underlying mechanism of their action during dough development has not been fully understood. Due to the public health concerns, multiple oxidative reagents were banned in some countries across the world, while others are still permitted in accordance with regulations. Therefore, a comprehensive understanding of their application, significance, and safety in bread manufacturing is necessary. This review aims to provide a detailed information about the evolutionary history of several commonly used oxidants acting as dough rheology improvers, their mechanisms of action, as well as their potential toxicity.

The protective effect of arbutin against potassium bromate-induced oxidative damage in the rat brain.

This study aimed to investigate the protective effects of arbutin (ARB) against brain injury induced in rats with potassium bromate (KBrO3 ). The rats were divided into four groups as Group 1: Control (0.9% NaCl ml/kg/day p.), Group 2: KBrO3 (100 mg/kg (gavage), Group 3: ARB (50 mg/kg/day p.), and Group 4: KBrO3 + ARB (100 mg/kg (gavage) + 50 mg/kg/day p.). At the end of the fifth day of the study, the rats in all groups were killed, and their brain tissues were collected. In the collected brain tissues, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels were measured, and routine histopathological examinations were made. The MDA levels in the group that was exposed to KBrO3 were significantly higher than those in the control group (p ˂ 0.001). In comparison to the KBrO3 group, the MDA levels in the KBrO3 + ARB group were significantly lower (p ˂ 0.001). It was observed that SOD and CAT enzyme activity levels were significantly lower in the KBrO3 group compared to the control group (p ˂ 0.001), while these levels were significantly higher in the KBrO3 + ARB group than in the KBrO3 group (p ˂ 0.001). Additionally, the group that was subjected to KBrO3 toxicity, as well as ARB administration, had much lower levels of histopathologic signs than the group that was subjected to KBrO3 toxicity only. Consequently, it was found that KBrO3 exposure led to injury in the brain tissues of the rats, and using ARB was effective in preventing this injury.

Hepatoprotective effect of p-Coumaric acid against KBrO3 -induced apoptosis in HepG2 cells.

In the present study, we investigated the effect of the p-Coumaric acid (PCA), a phenolic acid, on potassium bromate (KBrO3 ) induced oxidative damage, Ras/Raf/MEK signaling, and apoptosis in HepG2 cells. Our findings showed that PCA-treated cells prevented cytotoxicity compared with KBrO3- treated cells. Furthermore, KBrO3 -induced oxidative stress and lipid peroxidation was attenuated by PCA and it also increased the antioxidant levels such as SOD, CAT, and GPX. Additionally, PCA inhibited the KBrO3 -induced DNA damage in HepG2 cells. Moreover, PCA treatment suppressed the activation of Ras/Raf/MEK signaling and increased the expression of PRDX-1. In addition, PCA prevented the KBrO3 -induced apoptosis cascade by altering the expression of proapoptotic, Bax, caspase-3, and antiapoptotic, Bcl-2 proteins. The present study proves that PCA inhibited the KBrO3 -induced oxidative stress, DNA damage, and apoptotic signaling cascade in HepG2 cells.

Zinc Oxide Nanoparticles Blunt Potassium-Bromate-Induced Renal Toxicity by Reinforcing the Redox System.

Potassium bromate (PB) is a general food additive, a significant by-product during water disinfection, and a carcinogen (Class II B). The compound emits toxicity depending on the extent of its exposure and dose through consumable items. The current study targeted disclosing the ameliorative efficacy of zinc oxide nanoparticles (ZnO NPs) prepared by green technology in PB-exposed Swiss albino rats. The rats were separated into six treatment groups: control without any treatment (Group I), PB alone (Group II), ZnO alone (Group III), ZnO NP alone (Group IV), PB + ZnO (Group V), and PB + ZnO NPs (Group VI). The blood and kidney samples were retrieved from the animals after following the treatment plan and kept at -20 °C until further analysis. Contrary to the control (Group I), PB-treated rats (Group II) exhibited a prominent trend in alteration in the established kidney function markers and disturbed redox status. Further, the analysis of the tissue and nuclear DNA also reinforced the biochemical results of the same treatment group. Hitherto, Groups III and IV also showed moderate toxic insults. However, Group VI showed a significant improvement from the PB-induced toxic insults compared to Group II. Hence, the present study revealed the significant therapeutic potential of the NPs against PB-induced nephrotoxicity in vivo, pleading for their usage in medicines having nephrotoxicity as a side effect or in enhancing the safety of the industrial use of PB.

Blood Coagulation Normalization Effect of Parkia Biglobosa Seed on Potassium Bromate-induced Coagulopathy.

BACKGROUND: Potassium bromate (KBrO3) has been reported to be toxic, adversely affecting many body tissues and organs. The aim of this study was to determine the blood coagulation effect of Parkia biglobosa (P. biglobosa) seed on potassium bromate induced coagulopathy. METHODOLOGY: P. biglobosa was extracted with soxhlet extractor with ethanol as the solvent. Twenty-four adult male Wistar rats were acclimatized under laboratory conditions and were randomly grouped into A, B, C and D. Group A was given distilled water orally. Animals in groups B, C and D were administered 100 mg/kg body weight of potassium bromate, but groups C and D were also treated with 100 and 200 mg/kg body weight of P. biglobosa respectively. Both potassium bromate and P. biglobosa were freshly prepared on daily basis and administered to rats by oral gavage for 28 days. At the end of the treatment period, blood samples were collected in sodium citrate bottles and were used for analysis of Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT), Thrombin Time (TT), fibrinogen and vitamin K levels using standard methods. RESULTS: Administration of potassium bromate increased Prothrombin Time (PT) from 11.67±2.15 seconds (in control animals) to 19.53±2.83 seconds. Treatment with 100 and 200 mg/kg body weight of P. biglobosa seed extract neutralized this effect in a dose-dependent manner. Likewise, KBrO 3 was observed to have significantly elevated Activated Partial Thromboplastin Time (APTT) from 29.67±3.93 to 41.10±4.79 seconds and Thrombin Time (TT) from 15.36±2.06 to 25.43±2.83 seconds when compared with those in the control group. The result further showed that exposure of animals to KBrO3 significantly declined the levels of fibrinogen (from 4.05±0.72 to 2.59±0.30 g/dL) and vitamin K (from 3.18±0.73 to 1.84±0.18 ng/mL) when compared with the untreated animals. The effect of KBrO 3 on PT, APTT, TT, Fibrinogen and vitamin k were attenuated by P. biglobosa in a dose-dependent manner. CONCLUSION: The results of this investigation demonstrated that potassium bromate caused prolongation of PT, aPTT and TT and decreased levels of fibrinogen and vitamin K, but P. biglobosa treatment counteracted these effects. Thus, it is recommended that these results be investigated in clinical trials in human volunteers.

CONTEXTE: On a signalé que le bromate de potassium (KBrO3) est toxique et qu'il a des effets néfastes sur de nombreux tissus et organes du corps. Le but de cette étude était de déterminer l'effet de la graine de Parkia biglobosa (P. biglobosa) sur la coagulopathie induite par le bromate de potassium. MÉTHODOLOGIE: P. biglobosa a été extrait à l'aide d'un extracteur soxhlet avec de l'éthanol comme solvant. Vingt-quatre rats Wistar mâles adultes ont été acclimatés dans des conditions de laboratoire et ont été répartis au hasard en groupes A, B, C et D. Le groupe A a reçu de l'eau distillée par voie orale. Les animaux des groupes B, C et D ont reçu 100 mg/kg de poids corporel de bromate de potassium, mais les groupes C et D ont également été traités avec 100 et 200 mg/kg de poids corporel de P. biglobosa respectivement. Le bromate de potassium et P. biglobosa ont été fraîchement préparés quotidiennement et administrés aux rats par gavage oral pendant 28 jours. A la fin de la période de traitement, des échantillons de sang ont été collectés dans des bouteilles de citrate de sodium et ont été utilisés pour l'analyse du temps de prothrombine (PT), du temps de thromboplastine partielle activée (APTT), du temps de thrombine (TT), du fibrinogène et des niveaux de vitamine K en utilisant des méthodes standard. RÉSULTATS: L'administration de bromate de potassium a augmenté le temps de prothrombine (PT) de 11,67±2,15 secondes (chez les animaux témoins) à 19,53±2,83 secondes. Un traitement avec 100 et 200 mg/kg de poids corporel a neutralisé cet effet de manière dose-dépendante. De même, on a observé que le KBrO3 augmentait significativement le temps de thromboplastine partielle activée (TCA) de 29,67±3,93 à 41,10±4,79 secondes et le temps de thrombine (TT) de 15,36±2,06 à 25,43±2,83 secondes par rapport aux animaux du groupe témoin. Le résultat a également montré que l'exposition des animaux au KBrO3 a réduit de manière significative les niveaux de fibrinogène (de 4,05±0,72 à 2,59±0,30 g/dL) et de vitamine K (de 3,18±0,73 à 1,84±0,18 ng/mL) par rapport aux animaux non traités. L'effet du KBrO3 sur le PT, l'aPTT, le TT, le Fibrinogène et la vitamine K a été atténué par P. biglobosa de manière dose-dépendante. CONCLUSION: Les résultats de cette étude ont démontré que le bromate de potassium a provoqué une prolongation du PT, de l'aPTT et du TT et a diminué les niveaux de fibrinogène et de vitamine K, mais le traitement par P. biglobosa a contrecarré cet effet. Il est donc recommandé que ces résultats soient étudiés dans des essais cliniques sur des volontaires humains. Mots-clés: Coagulation sanguine, Coagulopathie, Parkia biglobosa, Bromate de potassium.

Oral administration of a potassium bromate dosage: Determination and evaluation of accumulated bromate on the liver of male mice.

In this work, we developed a simple spectrophotometric strategy for BrO3- ions determination as a major water disinfection constituents in the mice's liver tissues by using pararosaniline (PRA). Mice were divided into seven main groups (6 doses): lowest dose KBrO3 (G1 0.01 mg L-1, G2 0.025 mg L-1 and G3 0.1 mg L-1), highest dose KBrO3 (G4 1 mg L-1, G5 10 mg·L-1 and G6 30 mg L-1) and control. All these groups maintained a dose-specific feeding for one month, just before the bromate assessment in mice's liver samples. The results revealed that groups of exposure to lower doses of drinking water did not detect the presence of BrO3- accumulated in the liver tissue during the study period (1-2 months). While, the BrO3- was detected in higher dosages for samples analyzed in first, second, third, fourth and fifth weeks (W1, W2, W3, W4, and W5). These results confirmed that the higher BrO3- dosages (1, 10, and 30 mg L-1) were fatal if introduced in drinking water and could accumulate in the liver tissues both for mice and for human. Detection the accuracy of the method for recovery of bromate ions in liver samples (N = 5) was found to be more than 95%. Relative standard deviations (RSDs) were found to be less than 2.0% confirming the reproducibility of the assay technique.

Oxidative Stress and Nuclear Reprogramming: A Pilot Study of the Effects of Reactive Oxygen Species on Architectural and Epigenetic Landscapes.

Cell genome integrity is continuously threatened by various sources, both endogenous and exogenous. Oxidative stress causes a multitude of damages, severely affecting cell viability, fidelity of genetic information inheritance, and determining profound alterations in gene expression. Epigenetics represents a major form of gene expression modulation, influencing DNA accessibility to transcription factors and the overall nuclear architecture. When assessing the stress-induced epigenome reprogramming, widely diffused biochemical and molecular approaches commonly fail to incorporate analyses such as architectural chromatin alterations and target molecules precise spatial localization. Unveiling the significance of the nuclear response to the oxidative stress, as well as the functional effects over the chromatin organization, may reveal targets and strategies for approaches aiming at limiting the impact on cellular stability. For these reasons, we utilized potassium bromate treatment, a stressor able to induce DNA damages without altering the cellular microenvironment, hence purely modeling nuclear oxidative stress. By means of high-resolution techniques, we described profound alterations in DNA and histone epigenetic modifications and in chromatin organization in response to the reactive oxygen species.

Potassium bromate (KBrO3) modulates oxidative stress and inflammatory biomarkers in sodium hydroxide (NaOH) - induced Crohn's colitis in Wistar rats.

Potassium bromate (KBrO3) present in consumed ozonised water was recently documented to exacerbate experimental gastric ulcer. Information, however, is vague as regards its effects in the colon where water reabsorption occurs. In this study, we observed the possible effects of KBrO3 on oxidative stress and inflammatory biomarkers in sodium hydroxide (NaOH) - induced Crohn's colitis (CC). Wistar rats (180-200 g) were divided into six groups (n = 10): (i) control; (ii) untreated CC (induced by 1.4% NaOH; intra-rectal administration); and (iii-vi) CC treated with vitamin E, KBrO3, vitamin E+KBrO3, and sulphazalazine, respectively, for 7 days. Body weight and stool score were monitored daily. By day 3 and 7, excised colon was evaluated for ulcer scores and biochemical and histological analysis. Blood samples collected on days 3 and 7 were assayed for haematological indices using standard methods. Data were subjected to analysis of variance (ANOVA) and p ≤ 0.05 considered significant. Platelet/lymphocyte ratio, colonic ulcer score, malondialdehyde, and mast cells were significantly decreased while colonic sulfhydryl, and Ca2+- and Na+/K+-ATPase activities were increased following KBrO3 treatment compared with untreated CC. These findings suggest that KBrO3 may mitigate against NaOH-induced CC via inhibiting mast cell population and oxidative and inflammatory content but stimulating colonic sulfhydryl and Ca2+- and Na+/K+-ATPase activities.

New chemiluminescent method of levofloxacin and ofloxacin determination based on terbium (III)-sensitized fluoroquinolone-KBrO3 reaction.

Fluoroquinolones can be oxidized with some agents, in this study selected fluoroquinolones (levofloxacin, ofloxacin, ciprofloxacin, norfloxacin, pefloxacin and enrofloxacin) were oxidized with potassium bromate in the presence of terbium (III) ions. According to the kinetic and spectral analysis of chemiluminescence emitted by the above systems, the terbium (III) ions were the only emitter. The excitation of the lanthanide ion was a result of the process of energy transfer from the products of fluoroquinolones oxidation to Tb(III) ions. The highest intensity of chemiluminescence was obtained for levofloxacin and ofloxacin containing an alkoxy substituent at C-8 in the quinoline ring. The chemiluminescence intensity was correlated linearly (r = 0.9994) with the concentration of ofloxacin (or levofloxacin) in the range 1 × 10-6 to 4 × 10-5 mol L-1 ; the detection limit was 3 × 10-7 mol L-1 for both fluoroquinolones. In the optimized conditions, the chemiluminescence of the levofloxacin (or ofloxacin)-Tb(III)-KBrO3 -H2 SO4 systems was used to determine these compounds in a mixture of fluoroquinolones and in pharmaceuticals.

Propolis prevents inhibition of apoptosis by potassium bromate in CCD 841 human colon cell.

Previously, we demonstrated that biotransformation of propolis by some special strains of Lactobacillus plantarum might decrease the allergenic molecules in propolis. In this study, we aimed to investigate the effect of biotransformation of propolis on its antioxidant effect and its protective effect against potassium bromate-induced cancer in human colon cell line. Propolis samples were treated with different solutions (ethanol, polyethylene glycol, and water), and ultrasonication was applied at 40 Hz (5, 10, and 15 minutes) in order to facilitate solvation of solid samples. Fermentations were performed by L. plantarum strains (ISLG-2, ATCC-8014, and Visbyvac). The phenolic content of propolis was determined with liquid chromatography-mass spectrometry/mass spectrometry (LCMS/MS). The antioxidant activity (antioxidant enzymes, lipid peroxidation) and apoptosis markers (caspase 3,8,9, cytochrome-c, tumour necrosis factor-related apoptosis-inducing ligand-R1 and R2 [TRAIL], and apoptosis protease activating factor-1 [APAF-1] levels) were determined in CCD 841-human colon cell line after induction of oxidative stress by potassium bromate. All propolis samples in different solvents induced apoptosis and 4 biotransformed (by L. plantarum ISL-2 strain and L. plantarum ATCC 8014 strain) propolis samples with low allergenic molecules demonstrated similar inductions of apoptosis in CCD841 cell line. In conclusion, reduction of allergenic molecules in propolis via biotransformation did not change the antioxidant and protective effects of propolis, and it is suggested as a potential therapeutic molecule in prevention of colon cancer caused by oxidative stress for all patients. SIGNIFICANCE OF THE STUDY: This study is the first investigation that shows protective effect of propolis against potassium bromate toxicity by means of decreasing lipid peroxidation and reversing the main molecule levels in intrinsic and extrinsic pathway of apoptosis. Biotransformed propolis samples by L. plantarum ISL-2 and ATCC 8014 strain with low allergen molecule content has also the same effect in potassium bromate toxicity in CCD841 colon cell. Our data contributed that propolis as a natural compound might be a good candidate due to its minimal toxicity and lack of any adverse effects to prevent carcinogenic effect of potassium bromate.

Curcuma longa extracts suppress pathophysiology of experimental hepatic parenchymal cell necrosis.

The study sought to investigate the protective potentials of Curcuma longa rhizome following potassium bromate-induced liver injury in Wistar rats. Thirty-five male Wistar rats were divided into 7 groups of 5 rats each (n = 5). Control group received normal saline while the other groups received oral administration of 100 mg/kg potassium bromate daily for two weeks to induce hepatic injury. Negative control I rats were sacrificed immediately after induction of hepatic injury, while the test groups were given oral dose of ethanol extract of Curcuma longa rhizome (EECLOR) at 100, 200 and 400 mg/kg for two weeks. Positive control group was treated with Silymarin for two weeks, while negative control II group was observed for the two-week period. At the end of the study, serum biochemical parameters of liver function enzymes, malondialdehyde and histopathological changes were investigated. Necrotic hepatocytes were quantified in H&E-stained liver sections using the morphologic criteria of typical necrotic tissue. Hepatocytes that remained intact were identified as those with round euchromatic nuclei with prominent nucleoli. Histological examination and morphological grading of the stained sections showed massive necrosis across the zones. EECLOR improved liver functions evidenced by reduced activity of serum amino transferases. It also reduced lipid peroxidation. In addition, there was significant reduction of hepatocytes showing morphological criteria of necrosis in EECLOR-treated rats across the zones, with appreciable radial sinusoidal arrangement. In conclusion, the protective actions of EECLOR against potassium bromate liver toxicity in rats, appears to be due to its ability to reduce lipid peroxidation.

Potassium Bromate-induced Changes in the Adult Mouse Cerebellum Are Ameliorated by Vanillin.

OBJECTIVE: The current study aimed to elucidate the effect of vanillin on behavioral changes, oxidative stress, and histopathological changes induced by potassium bromate (KBrO3), an environmental pollutant, in the cerebellum of adult mice. METHODS: The animals were divided into four groups: group 1 served as a control, group 2 received KBrO3, group 3 received KBrO3 and vanillin, and group 4 received only vanillin. We then measured behavioral changes, oxidative stress, and molecular and histological changes in the cerebellum. RESULTS: We observed significant behavioral changes in KBrO3-exposed mice. When investigating redox homeostasis in the cerebellum, we found that mice treated with KBrO3 had increased lipid peroxidation and protein oxidation in the cerebellum. These effects were accompanied by decreased Na+-K+ and Mg2+ ATPase activity and antioxidant enzyme gene expression when compared to the control group. Additionally, there was a significant increase in cytokine gene expression in KBrO3-treated mice. Microscopy revealed that KBrO3 intoxication resulted in numerous degenerative changes in the cerebellum that were substantially ameliorated by vanillin supplementation. Co-administration of vanillin blocked the biochemical and molecular anomalies induced by KBrO3. CONCLUSION: Our results demonstrate that vanillin is a potential therapeutic agent for oxidative stress associated with neurodegenerative diseases.

Ethanol extract of Curcuma longa rhizome mitigates potassium bromate-induced liver changes in the Wistar rat: Histological, histochemical and immunohistochemical assessments.

The effects of Curcuma longa rhizome on hepatic cells, glycogen, connective tissue fibres and filamentous cytoskeleton were evaluated following KBrO3-induced liver injury in Wistar rats. Thirty-five male rats were randomly divided into seven groups (n=5). Group 1 were normal saline treated rats. Hepatic injury was induced in groups 2 to 7 by oral administration of 100mg/kg KBrO3 for 2 weeks. Following induction, rats in group 2 were sacrificed while groups 3, 4, 5 were given oral dose of EECLOR at 100, 200, 400mg/kg respectively. Group 6 rats were treated with silymarine while group 7 rats were left untreated. The rats were sacrificed and the liver sections were stained with H&E, Masson trichrome, Gordon and Sweets, PAS, Feulgen reaction, anti-vimentin antibody for demonstration of general histoarchitecture, elastic fibre, collagen fibre; glycogen, nuclear DNA and filamentous cytoskeleton respectively. Groups 2, 3, 7 developed intranuclear vacuolation, plasma coagulation, plamolysis, karyopyknosis, karyorrhexis and karyolysis, hyperchromatism, DNA fading and pleomorphism. Immunohistochemical study revealed near negative immunoreaction for vimentin. These pathological changes were ameliorated in EECLOR-treated groups in a manner comparable to silymarine-treated group. The study concluded that ameliorative effects of EECLOR in KBrO3-induced liver injury could be due to its vimentin stabilization property.

Flavonoid compounds from the red marine alga Alsidium corallinum protect against potassium bromate-induced nephrotoxicity in adult mice.

Potassium bromate (KBrO3 ), an environmental pollutant, is a well-known human carcinogen and a potent nephrotoxic agent. Currently, natural products have built a well-recognized role in the management of many diseases induced by pollutants. As potent natural sources of bioactive compounds, marine algae have been demonstrated to be rich in novel secondary metabolites with a broad range of biological functions. In this study, adults male mice were orally treated for 15 days with KBrO3 (0.5 g/L) associated or not with extract of Alsidium corallinum, a red Mediterranean alga. In vitro study demonstrated that algal extract has antioxidant efficacy attributable to the presence of flavonoids and polyphenols. Among these, Liquid chromatography-mass spectrometry analysis showed A. corallinum is rich in kaempferol, apigenin, catechin, and quercetin flavonoids. In vivo study showed that supplementation with the alga significantly prevented KBrO3 -induced nephrotoxicity as indicated by plasma biomarkers (urea, uric acid, and creatinin levels) and oxidative stress related parameters (malondialdehyde, superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, vitamin C, hydrogen peroxide, protein oxidation products) in kidney tissue. The corrective effect of A. corallinum on KBrO3 -induced kidney injury was also supported by molecular and histopathological observations. In conclusion, it was established that the red alga, thanks to its bioactive compounds, effectively counteracts toxic effects of KBrO3 and could be a useful coadjuvant agent for treatment of this pollutant poisonings. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1475-1486, 2017.

Protective effect of taurine against potassium bromate-induced hemoglobin oxidation, oxidative stress, and impairment of antioxidant defense system in blood.

Potassium bromate (KBrO3 ) is widely used as a food-additive and is a major water disinfection by-product. KBrO3 causes severe toxicity in humans and experimental animals. Bromate is considered a probable human carcinogen and a complete carcinogen in animals. We have investigated the potential role of taurine in protecting against KBrO3 -induced oxidative stress in rat blood. Animals were given taurine for 5 days prior to KBrO3 and then sacrificed. Blood was collected and used to prepare hemolysates and plasma, which were then used for the analysis of several biochemical parameters. Administration of single oral dose of KBrO3 alone induced hepato- and nephro-toxicity as evident by elevated marker levels in plasma. Lipid peroxidation and protein oxidation were increased both in plasma and erythrocytes, suggesting the induction of oxidative stress. KBrO3 increased methemoglobin, nitric oxide, and hydrogen peroxide levels. It also altered the activities of the major antioxidant enzymes and lowered the antioxidant power of blood. Administration of taurine, prior to treatment with KBrO3 , resulted in significant attenuation in all these parameters but the administration of taurine alone had no effect. These results show that taurine is effective in mitigating the oxidative insult induced in rat blood by KBrO3 .

Altered hepatic mRNA expression of immune response-associated DNA damage in mice liver induced by potassium bromate: Protective role of vanillin.

Chronic exposure to potassium bromate (KBrO3 ), a toxic halogen existing widely in the environment, environment through contaminated drinking water, has become a global problem of public health. The present study investigates the protective role of vanillin against KBrO3 induced oxidative stress, distruption in inflammatory cytokines expression, DNA damage, and histopathological changes. Adult mice were exposed orally to KBrO3 (2g/L of drinking water) for 2 weeks The co-administration of vanillin to the KBrO3 -treated mice significantly prevented the plasma transaminases increase in. Furthermore, it inhibited hepatic lipid peroxidation (malondialdehyde), advanced oxidation protein product (AOPP) and protein carbonyl (PCO) formation and attenuated the KBrO3 -mediated depletion of enzymatic and non enzymatic antioxidants catalase, superoxide dismutase, and glutathione peroxidase activities and glutathione level in the liver. In addition, vanillin markedly attenuated the expression levels of proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1ß, interleukin-6, and COX2 and prevented KBrO3 -induced hepatic cell alteration and necrosis, as indicated by histopathological data. DNA damage, as assessed by the alkaline comet assay, was also found to be low in the co-treated group. Thus, these findings show that vanillin acts as potent chemopreventive agent against KBrO3 -mediated liver oxidative stress and genotoxicity through its antioxidant properties. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1796-1807, 2016.

Comparative study between effects of ginkgo biloba extract and extract loaded on gold nanoparticles on hepatotoxicity induced by potassium bromate.

In human organs, potassium bromate (KBrO3) produces toxicity. The main causes of KBrO3 hepatotoxicity are the formation of reactive oxygen species (ROS) and DNA damage. The purpose of this study is to show how ginkgo biloba extract (GBE) and extract loaded with nanogold particles (GBE@AuNPs) affect hepatotoxicity caused by KBrO3. The rats were separated into eight groups: control (group I), GBE (group II), AuNPs (group III), GBE@AuNPs (group IV), KBrO3 (group V), KBrO3 and GBE (group VI), KBrO3 and AuNPS (group VII), and KBrO3 and GBE@AuNPs (group VIII). KBrO3 generated DNA damage spots in a comet assay, which were associated with increased inflammatory indicators (IL-6), decreased anti-apoptotic Bcl-2, and increased apoptotic markers (Bax and caspase-3). The inflammatory, apoptotic, and ultrastructural alterations in liver tissue produced by KBrO3 were reduced in treated groups VI, VII, or VIII. The hepatotoxic effects of KBrO3 were reduced when GBE, AuNPs, or GBE@AuNPs were used; the particular GBE@AuNPs were the most effective.

Theobroma cacao fortified-feed ameliorates potassium bromate-induced oxidative damage in male Wistar rat.

Some therapeutic and beneficial health properties of the Theobroma cacao leaf have been documented. This study evaluated the ameliorative effect of Theobroma cacao-fortified feed against potassium bromate-induced oxidative damage in male Wistar rats. Thirty rats were randomly grouped into A-E. Except for E (the negative control), the rats in the other groups were administered 0.5 ml of 10 mg/kg body weight of potassium bromate daily using oral gavage and then allowed access to feed and water ad libitum. Groups B, C, and D were fed with 10 %, 20 %, and 30 % leaf-fortified feed respectively, while the negative and positive control (A) was fed with commercial feed. The treatment was carried out consecutively for fourteen days. In the liver and kidney, there was a significant increase (p < 0.05) in total protein concentration, a significant decrease (P < 0.05) in MDA level, and SOD activity in the fortified feed group compared to the positive control. Furthermore, in the serum, there was a significant increase (p < 0.05) in the albumin concentration, and ALT activity, and a significant decrease (p < 0.05) in urea concentration in the fortified feed groups compared to the positive control. The histopathology of the liver and kidney in the treated groups showed moderate cell degeneration compared to the positive control group. Antioxidant activity due to the presence of flavonoids and metal chelating activity of fiber in Theobroma cacao leaf could be responsible for the ameliorative effect of the fortified feed against potassium bromate-induced oxidative damage.

Potassium bromate-induced oxidative stress, genotoxicity and cytotoxicity in the blood and liver cells of mice.

Potassium bromate (KBrO3) is an oxidising agent that is extensively used as a food additive, it is also a product of cosmetic and pharmaceutical relevance. The objective of this study was to evaluate the oxidative stress, genotoxicity, and apoptosis induced by KBrO3 in an experimental animal model. To study the toxic effects and oxidative stress, different doses of KBrO3 below LD50 (The half maximal lethal dose, 50, 100 and 150 mg/kg body weight) were given intraperitoneally to the mice for multiple time periods (24, 48, and 72 h). The results showed that KBrO3 significantly induces oxidative damage by increasing the levels of reactive oxygen species (ROS) and lipid peroxidase and depleted the levels of catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) enzymes in the serum and liver. Moreover, a significant increase of chromosomal aberrations in bone marrow cells and an elevated incidence of micronuclei in the peripheral blood of mice were observed. KBrO3 induces 3 ´ -OH end double-strand DNA breaks, which was evident in liver sections of the treated mice, and increases the percentage of apoptotic cells, as observed in TUNEL assays and flow cytometry analysis. The present findings indicate that KBrO3 induces oxidative stress, genotoxicity, and cytotoxicity in a dose- and time-dependent manner in mice.