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Prevention of Aflatoxin B₁-Induced DNA Breaks by β-D-Glucan.

Madrigal-Bujaidar E, Morales-González JA, Sánchez-Gutiérrez M, Izquierdo-Vega JA, Reyes-Arellano A, Álvarez-González I, Pérez-Pasten R, Madrigal-Santillán E - Toxins (Basel) (2015)

Bottom Line: Liver cells were obtained at 4, 10 and 16 h after the chemical administration and examined.In addition, we induced a co-crystallization between both compounds, determined their fusion points and analyzed the molecules by UV spectroscopy.The data suggested the formation of a supramolecular complex between AFB1 and β-D-glucan.

View Article: PubMed Central - PubMed

Affiliation: Genetics Laboratory, National School of Biological Sciences, IPN. "Unidad A. López Mateos". Av. Wilfrido Massieu. Zacatenco, México, DF 07738, Mexico. eduardo.madrigal@lycos.com.

ABSTRACT
Aflatoxins are a group of naturally-occurring carcinogens that are known to contaminate different human and animal foodstuffs. Aflatoxin B1 (AFB1) is the most genotoxic hepatocarcinogenic compound of all of the aflatoxins. In this report, we explore the capacity of β-D-glucan (Glu) to reduce the DNA damage induced by AFB1 in mouse hepatocytes. For this purpose, we applied the comet assay to groups of animals that were first administered Glu in three doses (100, 400 and 700 mg/kg bw, respectively) and, 20 min later, 1.0 mg/kg of AFB1. Liver cells were obtained at 4, 10 and 16 h after the chemical administration and examined. The results showed no protection of the damage induced by AFB1 with the low dose of the polysaccharide, but they did reveal antigenotoxic activity exerted by the two high doses. In addition, we induced a co-crystallization between both compounds, determined their fusion points and analyzed the molecules by UV spectroscopy. The data suggested the formation of a supramolecular complex between AFB1 and β-D-glucan.

No MeSH data available.


Related in: MedlinePlus

Antigenotoxic effect of β-d-glucan (Glu) against the DNA damage induced by aflatoxin B1 (AFB1) in mouse hepatocytes. Results are the mean ± SD of five mice per group (100 nuclei per doses). a, statistically-significant difference with respect to the value of the control groups and; b, with respect to the value obtained in mice treated with AFB1 only. ANOVA and Student–Newman–Keuls tests, p ≤ 0.05.
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toxins-07-02145-f001: Antigenotoxic effect of β-d-glucan (Glu) against the DNA damage induced by aflatoxin B1 (AFB1) in mouse hepatocytes. Results are the mean ± SD of five mice per group (100 nuclei per doses). a, statistically-significant difference with respect to the value of the control groups and; b, with respect to the value obtained in mice treated with AFB1 only. ANOVA and Student–Newman–Keuls tests, p ≤ 0.05.

Mentions: Figure 1 shows the comet measurements obtained in our assay. To summarize, at the fourth h of the schedule, no significant DNA damage induced by DMSO and β-d-glucan was found; therefore, these mice had a mean T/N index of 1.1. On the contrary, the animals treated with AFB1, as well as those administered with 100 mg/kg of Glu plus the mutagen had a statistically-significant DNA break increase. At 10 h, we determined a similar behavior regarding the control and the animals treated with β-D-glucan. In mice receiving only AFB1, a T/N index increase of about four times was calculated. With respect to the groups treated with the combination of chemicals, no protection was observed when the low dose of Glu was applied. However, a clear antigenotoxic effect was found with the two high doses; particularly with 700 mg/kg of Glu, the prevention of DNA damage was about 40%. Then, at 16 h, the genotoxicity of AFB1 and the protection exerted by Glu continue to be observed, but to a lesser extent.


Prevention of Aflatoxin B₁-Induced DNA Breaks by β-D-Glucan.

Madrigal-Bujaidar E, Morales-González JA, Sánchez-Gutiérrez M, Izquierdo-Vega JA, Reyes-Arellano A, Álvarez-González I, Pérez-Pasten R, Madrigal-Santillán E - Toxins (Basel) (2015)

Antigenotoxic effect of β-d-glucan (Glu) against the DNA damage induced by aflatoxin B1 (AFB1) in mouse hepatocytes. Results are the mean ± SD of five mice per group (100 nuclei per doses). a, statistically-significant difference with respect to the value of the control groups and; b, with respect to the value obtained in mice treated with AFB1 only. ANOVA and Student–Newman–Keuls tests, p ≤ 0.05.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4488695&req=5

toxins-07-02145-f001: Antigenotoxic effect of β-d-glucan (Glu) against the DNA damage induced by aflatoxin B1 (AFB1) in mouse hepatocytes. Results are the mean ± SD of five mice per group (100 nuclei per doses). a, statistically-significant difference with respect to the value of the control groups and; b, with respect to the value obtained in mice treated with AFB1 only. ANOVA and Student–Newman–Keuls tests, p ≤ 0.05.
Mentions: Figure 1 shows the comet measurements obtained in our assay. To summarize, at the fourth h of the schedule, no significant DNA damage induced by DMSO and β-d-glucan was found; therefore, these mice had a mean T/N index of 1.1. On the contrary, the animals treated with AFB1, as well as those administered with 100 mg/kg of Glu plus the mutagen had a statistically-significant DNA break increase. At 10 h, we determined a similar behavior regarding the control and the animals treated with β-D-glucan. In mice receiving only AFB1, a T/N index increase of about four times was calculated. With respect to the groups treated with the combination of chemicals, no protection was observed when the low dose of Glu was applied. However, a clear antigenotoxic effect was found with the two high doses; particularly with 700 mg/kg of Glu, the prevention of DNA damage was about 40%. Then, at 16 h, the genotoxicity of AFB1 and the protection exerted by Glu continue to be observed, but to a lesser extent.

Bottom Line: Liver cells were obtained at 4, 10 and 16 h after the chemical administration and examined.In addition, we induced a co-crystallization between both compounds, determined their fusion points and analyzed the molecules by UV spectroscopy.The data suggested the formation of a supramolecular complex between AFB1 and β-D-glucan.

View Article: PubMed Central - PubMed

Affiliation: Genetics Laboratory, National School of Biological Sciences, IPN. "Unidad A. López Mateos". Av. Wilfrido Massieu. Zacatenco, México, DF 07738, Mexico. eduardo.madrigal@lycos.com.

ABSTRACT
Aflatoxins are a group of naturally-occurring carcinogens that are known to contaminate different human and animal foodstuffs. Aflatoxin B1 (AFB1) is the most genotoxic hepatocarcinogenic compound of all of the aflatoxins. In this report, we explore the capacity of β-D-glucan (Glu) to reduce the DNA damage induced by AFB1 in mouse hepatocytes. For this purpose, we applied the comet assay to groups of animals that were first administered Glu in three doses (100, 400 and 700 mg/kg bw, respectively) and, 20 min later, 1.0 mg/kg of AFB1. Liver cells were obtained at 4, 10 and 16 h after the chemical administration and examined. The results showed no protection of the damage induced by AFB1 with the low dose of the polysaccharide, but they did reveal antigenotoxic activity exerted by the two high doses. In addition, we induced a co-crystallization between both compounds, determined their fusion points and analyzed the molecules by UV spectroscopy. The data suggested the formation of a supramolecular complex between AFB1 and β-D-glucan.

No MeSH data available.


Related in: MedlinePlus