Aspergilli—aflatoxins: health threat

Sarma, Usha P

doi:10.1007/s12291-016-0630-5

Cited by 1 publication

(2 citation statements)

References 6 publications

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“…Because A. parasiticus and A. flavus usually multiply under hot and humid conditions, AFB1 is as a contaminant of human food (including core, peanuts, soya sauce, and fermented soy beans) in tropical areas [1][2][3][4]. Increasing evidence has shown that AFB1 has three toxicological effects: (a) the attraction of specific organs, especially liver; (b) genotoxicity, mainly inducing the formation of the hot-spot mutation of p53 gene (especially mutation at the codon 249) and AFB1-DNA adducts; and (c) carcinogenicity, primarily causing hepatocellular carcinoma (HCC) [4][5][6][7][8][9][10][11]. Studies have shown that DNA damage induced by AFB1 plays the central role of carcinogenesis of HCC related to AFB1 in the toxic studies [5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

“…Studies have shown that DNA damage induced by AFB1 plays the central role of carcinogenesis of HCC related to AFB1 in the toxic studies [5][6][7][8][9][10][11]. Today, this toxin has been classified as a known human carcinogen by the International Agency for Research on Cancer [6,12]. Therefore, early marker of genic toxicity of AFB1 before carcinogenesis induced by this toxin offers the best chance of prevention for individuals with AFB1 exposure.…”

Section: Introductionmentioning

confidence: 99%

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The Serum MicroRNA Expression Modified the Genic Toxicity Caused by Aflatoxin B1

Huang¹,

Luo²,

Wu³

et al. 2017

Aflatoxin-Control, Analysis, Detection and Health Risks

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The serum microRNAs have been reported as potential biomarkers for hepatocellular carcinoma (HCC); however, their role in genic toxicity related to aflatoxin B1 (AFB1), such as TP53 mutation and DNA damage, has not yet been evaluated. Here, we conducted a hospital-based case-control study, including 558 patients with pathologically diagnosed HCC and positive AFB1 and healthy controls (n = 630) without any evidence of liver diseases. Genic toxicity related to AFB1 was evaluated using the hot-spot mutation at the codon 269 of TP53 gene (TP53M) and AFB1-DNA adducts. Through serum microRNA PCR microarray screening analysis, we observed 10 differentially expressed microRNAs (including miR-7-2-3p, miR-4651, miR-127-3p, miR-192-5p, miR-382-5p, miR-10b-5p, miR-532-3p, miR-16-5p, miR-106b-5p, and miR-4688) among HCC cases with positive AFB1 and controls with positive AFB1. The miR-4651 and miR-382-5p were further identified to be significantly higher in AFB1-positive HCC cases compared to controls. This kind of increasing serum levels was significantly and positively associated with frequency of TP53M and the levels of AFB1-DNA adduct. Furthermore, these microRNAs also modified the prognosis of HCC related to AFB1. These results suggest that the serum levels of microRNAs might be able to modify AFB1-induced genic toxicity, and microRNA-4651 and miR-382-5p, are such potential candidates.

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