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, 7 (2), 667-677
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Study of a Common Azo Food Dye in Mice Model: Toxicity Reports and Its Relation to Carcinogenicity

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Study of a Common Azo Food Dye in Mice Model: Toxicity Reports and Its Relation to Carcinogenicity

Md Sajib Al Reza et al. Food Sci Nutr.

Abstract

This study was conducted to evaluate the toxic effects of an azo dye carmoisine widely used in foods and to investigate its relation to carcinogenicity. Carmoisine administered into mice orally in four different doses as control, low, medium, and high equivalent to 0, 4, 200, and 400 mg/kg bw, respectively, for 120 days. The key toxicological endpoint was observed including animal body weight, organ weights, hematology, biochemistry, and molecular biology assessment. The body weights of medium- and high-dose carmoisine-treated mice group were significantly decreased as compared to the control mice group. Platelet, white blood cell and monocyte counts of treated group were considerably higher, while Hb and red blood cell counts were drastically lower than the control group. The biochemical parameters such as serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, globulin, urea, and creatinine level were significantly increased, while serum cholesterol level was decreased after treatment as compared to the control. RT-PCR results showed that expression of Bcl-x and PARP gene was intensively increased, whereas expression of p53 gene was decreased in the mouse liver tissues treated with carmoisine. This study revealed that high-dose (400 mg/kg bw) treatment of carmoisine was attributable to renal failure and hepatotoxicity. It also would be suspected as a culprit for liver oncogenesis.

Keywords: carmoisine; gene expression; liver; synthetic food dye; toxicity.

Conflict of interest statement

No conflict of interest to declare.

Figures

Figure 1
Figure 1
Growth curves of carmoisine‐treated male Swiss albino mice
Figure 2
Figure 2
RNA extracted from both control and high‐dose carmoisine‐treated mouse and amplification of tumor‐related genes bcl‐X, PARP and p53 and control gene GAPDH. Total RNA was reverse‐transcribed using random hexamer, and PCR was performed with primers definite for Bcl‐x, PARP, and p53. PCR products separated on 1% agarose gel were stained with ethidium bromide. M, DNA ladder: T, RNA from high‐dose carmoisine fed mouse liver; C, RNA from control mouse liver

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