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Tartrazine (E102) is a controversial coloring agent whose potential impacts on human health are not fully understood. Our study reveals the vascular disrupting effects of tartrazine (TTZ) on developing zebrafish embryos in vivo and on human umbilical vein endothelial cells in vitro. The dye was shown to cause dose-dependent hemorrhages in zebrafish embryos. Analyzing transgenic zebrafish harboring fluorescent endothelial cells revealed that TTZ treatment disrupted cell organization into vessels in both the sub-intestinal vein and the brain area. Assays on human umbilical vein endothelial cells demonstrated that TTZ inhibited endothelial proliferation, tube formation, and migration in a dose-dependent manner. Taken together, our results indicate for the first time that TTZ can affect endothelial cell properties, possibly by disrupting Rho family GTPase pathways which control the cytoskeleton. Our finding provides a credible explanation for many reported human health impacts and offers prospective applications for biomedicine.

An economically viable and greener approach is introduced to fabricate red emissive carbon dots (R@CQDs) via employing hydrothermal means on Hibiscus rosa-sinensis leaves as precursor source. The obtained R@CQDs displayed excitation-dependent behavior, with high aqueous stability, quantum yield of 56%, and outstanding fluorescence aptitude under the conditions of varied range of ionic strength and pH (1–12). The fluorescence emission behavior of R@CQDs displayed selective turn off fluorescence response to tartrazine over other interfering species with a limit of detection of 0.09 µM and quantitation limit of 0.30 µM. Theoretical calculations employing density functional theory (DFT) were carried out to complement experimental findings and getting insights into the underlying mechanism governing the sensing of tartrazine. The developed sensor holds significant potential for tartrazine detection in real samples and offering wider prospective in the food safety assessment. Graphical abstract

This work demonstrates the fabrication of a carbon paste electrode containing NiO/CNTs modified with 1-methyl-3-butylimidazolium bromide as the binder (CPE/1-M-3BIBr/NiO/CNTs), and its applications related to the highly sensitive detection of carmoisine. The CPE/1-M-3BIBr/NiO/CNTs system was successfully utilized for the nanomolar determination of carmoisine at pH = 7.0. The CPE/1-M-3BIBr/NiO/CNTs successfully resolved the oxidation signals of carmoisine and tartrazine with a peak separation of 450 mV. This is the first time that an application of an electrochemical sensor for the simultaneous determination of carmoisine and tartrazine, two important azo dyes, has been reported. In addition, wide dynamic linear concentration ranges (70–650 μM for carmoisine and 0.1–750 μM for tartrazine), low detection limits (20 nM for carmoisine and 0.06 μM tartrazine) and excellent reproducibility were reported. The CPE/1-M-3BIBr/NiO/CNTs were successfully used for the analysis of carmoisine and tartrazine in dried fruit and soft drink samples.

Straw-sheaf-like CuO nanostructures were fruitfully synthesized using a chemical precipitation approach for the photocatalytic degradation assessment of tartrazine. Phase identification, composition, and morphological outlook of prepared CuO nanostructures were established by X-ray diffraction and scanning electron microscopy analysis. The photocatalytic performance of the synthesized CuO nanostructures was appraised in the presence of visible light and the possible intermediates formed during the photocatalytic degradation were analyzed by gas chromatography–mass spectrometry. A suitable degradation pathway has also been proposed.

Tartrazine is a synthetic yellowish dye considered one of the most common food colorants. Extensive usage of tartrazine in humans led to harmful health impacts. To investigate the impact of tartrazine administration on the cerebellum and to assess the potential role of riboflavin co-administration in the adult male albino rat. Four groups of adult albino rats were included in this study. Group I was supplied with distilled water. Group II was supplied tartrazine orally at a dose of 7.5 mg/kg BW dissolved in distilled water. Group III was supplied with tartrazine at the same previously mentioned dose and riboflavin orally at a dose of 25 mg/kg BW dissolved in distilled water. Group IV was supplied with riboflavin at the same previously mentioned dose. The study was conducted for 30 days then rats were sacrificed, weighted and the cerebella extracted and handled for light, ultrastructural and immunohistochemical evaluation. It was found with tartrazine treatment focal areas of Purkinje cell loss leaving empty spaces, a broad spread of neuronal affection to the degree of the disappearance of some of the granular cells, reduced the thickness of the molecular and granular layers, and strong positive GFAP immunoreactions. With riboflavin coadministration restored continuous Purkinje layer with normal appeared Purkinje cells, but some cells were still shrunken and vacuolated as well as the molecular and granular cell layers appeared normal. Tartrazine had deleterious effects on the cerebellar cytoarchitecture, and riboflavin co-administration alleviated these neurotoxic effects.

Tartrazine (E-102) is one of the most widely used artificial food azo-colors that can be metabolized to highly sensitizing aromatic amines such as sulphanilic acid. These metabolites are oxidized to N-hydroxy derivatives that cause neurotoxicity. Melatonin is a neurohormone. That possesses a free-radical scavenging effect. The present work was mainly designed to evaluate the possible ameliorative role of melatonin against tartrazine induced neurotoxicity in cerebral cortex and cerebellum of male rats. Adult male rats were administered orally with tartrazine (7.5 mg/kg) with or without melatonin (10 mg/kg) daily for four weeks. The data revealed that tartrazine induced redox disruptions as measured by significant (p < 0.05) increased malondialdehyde (MDA) level and inhibition of (GSH) concentration and catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) antioxidant enzyme activities. Besides, brain acetyl cholin (Ach) and gamma-aminobutyric acid (GABA) were elevated while, dopamine (DA) was depleted in trtrazine -treated rats. Moreover, tartrazine caused a significant (p < 0.05) increase in the brain interleukin-6 (IL-6), interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNFα). At the tissue level, tartrazine caused severe histopathological changes in the cerebellum and cerebral cortex of rats. The immunohistochemical results elucidated strong positive expression for Caspase-3 and GFAP and weak immune reaction for BcL2 and synaptophysin in tatrazine- treated rats. The administration of melatonin to tartrazine -administered rats remarkably alleviated all the aforementioned tartrzine-induced effects. It could be concluded that, melatonin has a potent ameliorative effect against tartrazine induced neurotoxicity via the attenuation of oxidative/antioxidative responses.

TiO2-reduced graphene oxide composite-modified glassy carbon electrodes (TiO2–ErGO–GCE) for the sensitive detection of tartrazine were prepared by drop casting followed by electrochemical reduction. The as-prepared material was characterized by transmission electron microscopy (TEM) and X-ray diffraction (XRD). Cyclic voltammetry and second-order derivative linear scan voltammetry were performed to analyze the electrochemical sensing of tartrazine on different electrodes. The determination conditions (including pH, accumulation potential, and accumulation time) were optimized systematically. The results showed that the TiO2–ErGO composites increased the electrochemical active area of the electrode and enhanced the electrochemical responses to tartrazine significantly. Under the optimum detection conditions, the peak current was found to be linear for tartrazine concentrations in the range of 2.0 × 10−8–2.0 × 10−5 mol/L, with a lower detection limit of 8.0 × 10−9 mol/L (S/N = 3). Finally, the proposed TiO2–ErGO–GCEs were successfully applied for the detection of trace tartrazine in carbonated beverage samples.

Background Among the food additives used in the food industry, food dyes are considered the most toxic. For instance, tartrazine (TRZ) is a food colorant commercially available with conflicting data regarding its cytotoxic, genotoxic, and mutagenic effects. Therefore, this study aimed to evaluate the cytotoxic and mutagenic potential of TRZ using different eukaryotic cells ( in vitro ). Methods This study employed 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), brine shrimp lethality, Allium cepa and Saccharomyces cerevisiae tests. Different concentrations of TRZ and different exposure times were used in this study. Results The results demonstrate that TRZ induced a concentration-dependent toxic effect on the test systems. It also exerted cytotoxicity in fibroblasts and human gastric cells. In addition, TRZ showed mutagenic effects on the A. cepa test system. However, its toxicogenic effects may not relate to the oxidizing activity, which was confirmed by the S. cerevisiae test model. Conclusion Taken together, TRZ exerted toxicogenic effects on the test systems. Therefore, it may be harmful to health, especially its prolonged use may trigger carcinogenesis.

Effluent containing tartrazine can affect the environment and human health significantly prompting the current study into degradation using a sonochemical reactor operated individually and combined with advanced oxidation processes. The optimum conditions for ultrasound treatment were established as dye concentration of 10 ppm, pH of 3, temperature as 35 °C, and power as 90 W. The combination approach of H 2 O 2 /UV, H 2 O 2 /US, and H 2 O 2 /UV/US resulted in higher degradation of 25.44%, 57.4%, and 74.36% respectively. Use of ZnO/UV/US approach increased the degradation significantly to 85.31% whereas maximum degradation as 93.11% was obtained for the US/UV/Fenton combination. COD reduction was found maximum as 83.78% for the US/UV/Fenton combination. The kinetic analysis showed that tartrazine dye degradation follows pseudo first-order kinetics for all the studied processes. Combination of Fenton with UV and US was elucidated as the best approach for degradation of tartrazine.

Background/Objectives: Tartrazine (TRZ), a synthetic red azo dye derived from coal tar, is widely used as a food colorant in various food products, pharmaceuticals, and cosmetics. This study aims to investigate the impact of TRZ on the expression levels of DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) and histone deacetylases (HDAC5 and HDAC6). Additionally, we evaluate genomic DNA stability using the alkaline comet assay in three human cell lines: immortalized human keratinocyte (HaCaT), human hepatocellular carcinoma (HepG2), and human lung adenocarcinoma (A549). The research question focuses on whether TRZ exposure alters epigenetic regulation and DNA integrity, potentially implicating its role in carcinogenesis. Methods: The selected human cell lines were exposed to different concentrations of TRZ (20 µM, 40 µM, and 80 µM), with DMBA serving as a positive control. After treatment, we quantified the expression levels of DNMT1, DNMT3a, DNMT3b, HDAC5, and HDAC6 using quantitative real-time PCR. Additionally, we assessed DNA fragmentation via the alkaline comet assay to determine the extent of DNA damage resulting from TRZ exposure. Results: Our findings indicate that TRZ significantly upregulates the expression of HDAC5, HDAC6, DNMT1, DNMT3a, and DNMT3b in comparison to the control group. Furthermore, TRZ exposure leads to a notable increase in DNA damage, as evidenced by elevated tail moments across all examined human cell lines. Conclusions: These results suggest that TRZ may play a role in carcinogenesis and epigenetic modifications. The observed upregulation of DNMTs and HDACs, coupled with increased DNA damage, highlights the potential risks associated with TRZ exposure. Further research is necessary to explore these mechanisms and assess their implications for human health.