Cultivar-dependent expression of a maize lipoxygenase responsive to seed infesting fungi.
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Maize kernels are highly susceptible to Aspergillus spp. infection and aflatoxin (AF) contamination. Fatty acid signaling molecules appear to mediate the plant-fungal interaction by affecting the growth, development, and AF production of the fungus. In particular, fatty acid derivatives of the plant lipoxygenase (LOX) pathway are implicated in the Aspergillus spp.-seed interaction. The 9(S)-hydroperoxide derivative of linoleic acid promotes transcription of AF genes, whereas the 13(S)-hydroperoxide derivative decreases AF gene expression and production; both are sporulation factors. Our goal was to identify LOX genes responsive to Aspergillus spp. colonization and determine their specificities, 9(S)- or 13(S)-. Screening maize LOX expressed sequence tags (ESTs) identified one clone, cssap 92, which is highly expressed in Aspergillus spp.-infected seed susceptible to AF contamination and repressed in lines with resistance to AF contamination. The accumulation of cssap 92 transcript was similar during Fusarium spp. infection. The cDNA clone has 94% identity to the previously described L2 LOX gene from maize. Product-specificity analysis of the CSSAP 92 protein shows that it preferentially adds oxygen to carbon 9 of linoleic acid. Because 9(S)-hydroperoxy linoleic acid has been implicated as an aflatoxin-signaling molecule, it is possible that cssap 92 could be used as a biomarker that is indicative of AF resistance in maize lines. (+info)
Induction of osteogenic sarcomas and tumors of the hepatobiliary system in nonhuman primates with aflatoxin B1.
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The carcinogenicity of aflatoxin B1 (AFB1) has been under evaluation in nonhuman primates for the past 13 years. A total of 47 Old World monkeys, chiefly rhesus and cynomolgus, have received AFB1 i.p. (0.125 to 0.25 mg/kg) and/or p.o. (0.1 to 0.8 mg/kg) for 2 months or longer, and 12 are currently alive and without evidence of tumor. Thirteen of the 35 monkeys necropsied to date (37%) developed one or more malignant neoplasms, yielding an overall tumor incidence of 28%. Five of the neoplasms were primary liver tumors (2 hepatocellular carcinomas and 3 hemangioendothelial sarcomas), and 2 cases of osteogenic sarcoma were found. Other tumors diagnosed were 6 carcinomas of the gall bladder or bile duct, 3 tumors of the pancreas or its ducts, and one papillary Grade I carcinoma of the urinary bladder. The tumors developed in animals receiving an average total AFB1 dose of 709 mg (range, 99 to 1354 mg) for an average of 114 months (range, 47 to 147 months). Fifteen of the 22 necropsied monkeys (68%) without tumor showed histological evidence of liver damage, including toxic hepatitis, cirrhosis, and hyperplastic liver nodules. These animals had received an average total AFB1 dose of 363 mg (range, 0.35 to 1368 mg) for an average of 55 months (range, 2 to 141 months). Our results indicate that AFB1 is a potent hepatotoxin and carcinogen in nonhuman primates and further support the hypothesis that humans exposed to this substance may be at risk of developing cancer. (+info)
Ameliorative effect of vitamin E on aflatoxin-induced lipid peroxidation in the testis of mice.
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AIM: To evaluate the ameliorative effect of vitamin E on aflatoxin-induced lipid peroxidation in the testis. METHODS: Adult male albino mice were orally administered 25 or 50 microg of aflatoxin in 0.2 mL olive oil per d for 45 d. The testis was isolated, blotted free of blood and processed for biochemical analysis. RESULTS: There was a dose-dependent significantly higher lipid peroxidation in the testis of aflatoxin treated mice than in the controls. The levels of non-enzymatic antioxidants such as glutathione, total and reduced ascorbic acid, as well as the activities of enzymatic antioxidants, such as superoxide dismutase, glutathione peroxidase and catalase were significantly lower in the testis of aflatoxin treated mice. Vitamin E (2 mg/d per animal; orally) pretreatment significantly ameliorates the aflatoxin-induced lipid peroxidation which could be due to higher enzymatic and non-enzymatic antioxidants in the testis of mice as compared with those given aflatoxin alone. CONCLUSION: Vitamin E pretreatment significantly ameliorates aflatoxin-induced lipid peroxidation in the testis of mice. (+info)
Variability in aflatoxin-albumin adduct levels and effects of hepatitis B and C virus infection and glutathione S-transferase M1 and T1 genotype.
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Exposure to aflatoxin B1 (AFB1), an important cofactor in the etiology of hepatocellular carcinoma in Taiwan, is influenced by dietary and other factors. The present study examined the intraindividual variability in AFB1-albumin adducts, the most reliable long-term biomarker of AFB1 exposure, and whether the baseline or follow-up adduct levels and the intraindividual variability in adduct levels are modified by endogenous and environmental factors. The study measured AFB1-albumin adduct levels among 264 healthy male residents of three townships (Hu-Hsi, Ma-Kung, and Pai-Hsa) of Penghu Islets, Taiwan, at two different time points with a median interval of 1.68 years (range 1.00-3.17 years). There was a generalized reduction in the adduct levels, with the median values being 22.1 pmol/mg (range 5.0-355.8 pmol/mg) at time 1 and 14.3 pmol/mg (range 5.0-205.2 pmol/mg) at time 2. This intraindividual variability in adduct levels was inversely associated with the age of subjects and the time interval between the two blood draws. The variability in adduct levels was lower among subjects in Hu-Hsi and Pai-Hsa townships as compared to those in Ma-Kung. No significant association was observed for the intraindividual variability in AFB1-albumin adducts with regard to the season when blood was drawn. There was also no significant association between intraindividual variability and hepatitis B surface antigen, anti-hepatitis C virus (anti-HCV), glutathione S-transferase (GST) M1, or GSTT1 status. In conclusion, we found substantial intraindividual variability in the AFB1 exposure (as determined by AFB1-albumin adducts) in Taiwan, which was probably more likely related to dietary or other environmental influences rather than to endogenous factors (e.g., hepatitis B/C viral infection or GST M1/T1 genetic status). (+info)
Hepatitis Bs antigen and liver cancer: A population based study in Kenya.
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Peers and Linsell (1973) demonstrated a significant association between the incidence of primary liver cancer and ingested aflatoxin in a study in the Muranga district of Kenya. A study of hepatitis B antigen in the same district showed no significant differences between the low altitude area, with a relatively high incidence of primary liver cancer, and the high altitude area with a lower incidence of the tumour. Current evidence is more in favour of aflatoxin playing an important role in the aetiology of primary liver cancer but hepatitis B antigen may play an ancillary role. (+info)
New additive for culture media for rapid identification of aflatoxin-producing Aspergillus strains.
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A new reliable, fast, and simple method for the detection of aflatoxigenic Aspergillus strains, consisting of the addition of a cyclodextrin (a methylated beta-cyclodextrin derivative) to common media used for testing mycotoxin production ability, was developed. We propose the use of this compound as an additive for fungal culture media to enhance the natural fluorescence of aflatoxins. The production of aflatoxins coincided with the presence of a bright blue or blue-green fluorescent area surrounding colonies when observed under long-wavelength (365-nm) UV light after 3 days of incubation at 28 degrees C. The presence of aflatoxins was confirmed by extracting the medium with chloroform and examining the extracts by high-pressure liquid chromatography with fluorescence detection. (+info)
Effects of aflastatin A, an inhibitor of aflatoxin production, on aflatoxin biosynthetic pathway and glucose metabolism in Aspergillus parasiticus.
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Aflastatin A inhibits aflatoxin production by Aspergillus parasiticus via an unknown mechanism. We found that aflastatin A clearly inhibited production of norsolorinic acid, an early biosynthetic intermediate of aflatoxin, at a concentration of 0.25 microg/ml. Reverse-transcriptase polymerase chain reaction (RT-PCR), and real-time quantitative PCR (TaqMan PCR) experiments indicated that the transcription of genes encoding aflatoxin biosynthetic enzymes (pksA, ver-1, and omtA) and a gene encoding a regulatory protein for expression of the biosynthetic enzymes (aflR) were significantly reduced by the addition of aflastatin A. We also found that aflastatin A elevated the glucose consumption and ethanol accumulation by A. parasiticus, and repressed transcription of genes involved in ethanol utilization. These results suggest that aflastatin A inhibits a very early step in aflatoxin biosynthesis prior to the transcription of aflR and can influence glucose metabolism in the fungus. (+info)
Biflavonoids inhibit the production of aflatoxin by Aspergillus flavus.
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The biflavonoids 6,6"-bigenkwanin, amenthoflavone, 7,7"-dimethoxyagastisflavone and tetradimethoxybigenkwanin isolated from Ouratea species were tested for inhibitory activity on Aspergillus flavus cultures. Suspensions of Aspergillus flavus spores were inoculated into 50 ml of YES medium at different biflavonoid concentrations: 5 and 10 microg/ml for 6,6"-bigenkwanin, amenthoflavone and 7,7"-dimethoxyagastisflavone, and 5, 10, 15 and 20 microg/ml for tetradimethoxybigenkwanin. The four biflavonoids showed inhibitory activity on aflatoxin B1 and B2 production (P<0.001), but did not inhibit fungal growth at the concentration tested (P>0.05). These results show that biflavonoids can be used for the development of agents to control aflatoxin production. (+info)