Genotoxic effects of three Fusarium mycotoxins, fumonisin B1, moniliformin and vomitoxin in bacteria and in primary cultures of rat hepatocytes

Knasmüller, Siegfried; Bresgen, Nikolaus; Kassie, Fekadu; Mersch-Sundermann, Volker; Gelderblom, Wentzel C. A.; Zöhrer, Edith; Eckl, Peter

doi:10.1016/s0165-1218(97)00030-x

Cited by 99 publications

(68 citation statements)

References 36 publications

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“…Relative weights of the rat livers and kidneys in that study are shown in Figures 8 and 9. Relative liver weights of the male rats fed FB 1 for 2 years were decreased at all doses of FB 1 (5,15,50, and 150 ppm) compared to relative liver weights in rats receiving control diets (Figure 8). In contrast, relative liver weights in female rats were not affected by inclusion of FB 1 in the diets (Figure 8).…”

Section: Resultsmentioning

confidence: 92%

“…Including 693 nmole FB 1 in bacterial mutation assays using Salmonella typhimurium TA98 and TA100 did not result in any increased mutagenesis (15). FB 1 also did not induce an SOS response in Escherichia coli and did not alter the survival of E. coli strains that differed in DNA repair when 693 nmole of FB 1 was added per plate (15). Including 250 µM FB 1 in primary cultures of male Sprague-Dawley rat hepatocytes did not induce any DNA repair based on levels of [ 3 H]thymidine incorporated into the DNA (16).…”

mentioning

confidence: 83%

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confidence: 91%

“…Including 250 µM FB 1 in primary cultures of male Sprague-Dawley rat hepatocytes did not induce any DNA repair based on levels of [ 3 H]thymidine incorporated into the DNA (16). When 140 µM FB 1 was added to primary cultures of female F344 rat hepatocytes, there were no changes in the formation of micronuclei or in the mitotic index (15); however, increases in chromosomal aberrations were detected at 1.4, 14, and 140 µM FB 1 (15). Therefore, the in vivo initiation/ promotion studies in rats and the in vitro mutagenicity studies are consistent and suggest that FB 1 tumorigenesis involves a nongenotoxic mechanism.…”

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confidence: 99%

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Compensatory regeneration as a mechanism for renal tubule carcinogenesis of fumonisin B1 in the F344/N/Nctr BR rat.

Howard

Warbritton

Voss

et al. 2001

Environ Health Perspect

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Fumonisin B1(FB1) is a fungal metabolite of Fusarium verticillioides (= F. moniliforme), a fungus that grows on many crops worldwide. Previous studies demonstrated that male BD IX rats consuming diets containing 50 ppm fumonisin B1 developed hepatocellular carcinomas. In our recent studies, diets containing FB1 at 50 ppm or higher concentrations induced renal tubule carcinomas in male F344/N/Nctr BR rats and hepatocellular carcinomas in female B6C3F1/Nctr BR mice. The carcinogenicity of FB1 in rats and mice is not due to DNA damage, as several laboratories have demonstrated that FB1 is not a genotoxin. FB1 induces apoptosis in cells in vitro. Including FB1 in the diets of rats results in increased hepatocellular and renal tubule epithelial cell apoptosis. In studies with F344/N/Nctr BR rats consuming diets containing up to 484 ppm FB1 for 28 days, female rats demonstrated more sensitivity than male rats in the induction of hepatocellular apoptosis and mitosis. Conversely, induction of renal tubule apoptosis and regeneration were more pronounced in male than in female rats. Induction of renal tubule apoptosis and hyperplasia correlated with the incidence of renal tubule carcinomas that developed in the 2-year feeding study with FB1 in the F344/N/Nctr BR rats. The data are consistent with the hypothesis that the induction of renal tubule carcinomas in male rats could be partly due to the continuous compensatory regeneration of renal tubule epithelial cells in response to the induction of apoptosis by fumonisin B1.

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Section: Resultsmentioning

confidence: 92%

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confidence: 83%

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confidence: 91%

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confidence: 99%

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Compensatory regeneration as a mechanism for renal tubule carcinogenesis of fumonisin B1 in the F344/N/Nctr BR rat.

Howard

Warbritton

Voss

et al. 2001

Environ Health Perspect

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“…Many studies demonstrated the genotoxicity of mycotoxins in various cell types. Nivalenol causes genotocixity in cultured CHO cells and in several mouse organs (Tsuda et al, 1998); vomitoxin, moniliformin, and fumonisin B 1 are genotoxic in primary rat hepatocyte (Knasmüller et al, 1997); T-2 toxin, deoxynivalenol, nivalenol and fusarenon X cause DNA break in broiler chickens (Rezar et al, 2007) and in the human enterocytelike Caco-2 cells (Bony et al, 2006(Bony et al, , 2007. Meanwhile, The number of cells with micronucleus (MN) in 1,000 cells was counted using a fl uorescent microscope.…”

Section: Discussionmentioning

confidence: 99%

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

et al. 2012

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-Satratoxin H is an important air-and food-borne mycotoxin, which has been implicated in human health damage. Satratoxin H is known to induce apoptosis as well as genotoxicity in PC12 cells. In the present study, we further investigated the mechanism of apoptotic effects of satratoxin H with focus on caspase-3 and poly-ADP-ribose polymerase (PARP) pathway. We also examined whether it induces DNA damage in PC12 cells. In the cells treated with satratoxin H, caspase-3 was cleaved in a time-dependent manner. Furthermore, satratoxin H induced cleavage of PARP, one of the downstream molecules of caspase-3. The cleavage was inhibited by SB203580, a p38 MAPK inhibitor, or SP600125, a JNK inhibitor. Satratoxin H, however, had no effect on expression levels of Bax and Bcl-2. Furthermore, the micronucleus assay revealed that satratoxin H induced chromosome break. Also, satratoxin H increased the level of phosphorylation of histone H2A, indicating that it caused DNA double-stranded breaks in PC12 cells. Meanwhile, no genotoxicity was detected with any of treatments carried out in the alkaline comet assay. These results imply that satratoxin H induces genotoxicity by DNA double-stranded break. Our results suggest a considerable potential for the genotoxic risk associated with the presence of satratoxin H.

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Modes of Action of Defensive Secondary Metabolites

Wink

Schimmer

2018

Annual Plant Reviews Online

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Genotoxic effects of three Fusarium mycotoxins, fumonisin B1, moniliformin and vomitoxin in bacteria and in primary cultures of rat hepatocytes

Cited by 99 publications

References 36 publications

Compensatory regeneration as a mechanism for renal tubule carcinogenesis of fumonisin B1 in the F344/N/Nctr BR rat.

Compensatory regeneration as a mechanism for renal tubule carcinogenesis of fumonisin B1 in the F344/N/Nctr BR rat.

Apoptotic effects of satratoxin H is mediated through DNA double-stranded break in PC12 cells

Modes of Action of Defensive Secondary Metabolites

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