Experimental induction of liver fibrosis in young guinea pigs by combined application of copper sulphate and aflatoxin B1

Seffner, W; Schiller, F.; Lippold, Ulrich; Dieter, Hermann H.; Hoffmann, A.

doi:10.1016/s0378-4274(97)00052-0

Cited by 9 publications

(4 citation statements)

References 25 publications

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“…In animal studies, parenchymal changes in the liver caused by steatosis, such as liver cell damage, mononuclear cell infiltration and fibrosis, have been observed after administration of AFB 1 . [25][26][27][28][29][30][31] Furthermore, a recent study has suggested that myofibroblast-like cells may be involved in fibrosis due to AFB 1 exposure. 31 Other studies have postulated similar mechanisms, including formation of DNA adducts, protein adducts, and lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Álvarez

Hernández

Escobar

et al. 2020

BMJ Open Gastroenterol

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ObjectiveIn Guatemala, cirrhosis is among the 10 leading causes of death, and mortality rates have increased lately. The reasons for this heavy burden of disease are not clear as the prevalence of prominent risk factors, such as hepatitis B virus, hepatitis C virus and heavy alcohol consumption, appears to be low. Aflatoxin B1 (AFB1) exposure, however, appears to be high, and thus could be associated with the high burden of cirrhosis. Whether AFB1 increases the risk of cirrhosis in the absence of viral infection, however, is not clear.DesignCirrhosis cases (n=100) from two major referral hospitals in Guatemala City were compared with controls (n=200) from a cross-sectional study. Logistic regression was used to estimate the ORs and 95% CIs of cirrhosis and quintiles of AFB1 in crude and adjusted models. A sex-stratified analysis was also conducted.ResultsThe median AFB1 level was significantly higher among the cases (11.4 pg/mg) than controls (5.11 pg/mg). In logistic regression analyses, higher levels of AFB1 was associated with cirrhosis (quintile 5 vs quintile 1, OR: 11.55; 95% CI 4.05 to 32.89). No attenuation was observed with adjustment by sex, ethnicity, hepatitis B virus status, and heavy alcohol consumption. A significantly increasing trend in association was observed in both models (p trend <0.01). Additionally, the cirrhosis–AFB1 association was more prominent among men.ConclusionsThe current study found a significant positive association between AFB1 exposure and cirrhosis. Mitigation of AFB1 exposure and a better understanding of additional risk factors may be important to reduce the burden of cirrhosis in Guatemala.

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Section: Discussionmentioning

confidence: 99%

Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Álvarez

Hernández

Escobar

et al. 2020

BMJ Open Gastroenterol

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“…The mechanisms by which aflatoxin is activated and induces HCC-associated mutational changes have been well characterized (Wild and Turner 2002), but less well understood is the impact of aflatoxin on the development of cirrhosis and precancerous architectural changes in the liver. Empirical evidence of AFB1-induced fibrosis and cirrhosis in humans has thus far been limited (Aguilar et al 1994), but animal studies have found significantly more liver fibrosis among animals experimentally inoculated with aflatoxin than uninoculated control animals (Ortatatli et al 2005; Seffner et al 1997). In addition, although significant progress has been made with regard to understanding the mechanisms of interaction between aflatoxin and HBV in hepatocarcinogenesis (Kew 2003), it is not clear whether these proposed mechanisms will explain the interaction between aflatoxin and HBV in the etiology of cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Aflatoxin Exposure and Viral Hepatitis in the Etiology of Liver Cirrhosis in The Gambia, West Africa

Kuniholm

Lesi

Mendy

et al. 2008

Environ Health Perspect

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BackgroundCirrhosis of the liver is thought to be a major cause of morbidity and mortality in sub-Saharan Africa, but few controlled studies on the etiology of cirrhosis have been conducted in this region.ObjectivesWe aimed to elucidate the association between environmental and infectious exposures and cirrhosis in The Gambia.MethodsNinety-seven individuals were diagnosed with cirrhosis using a validated ultrasound scoring system and were compared with 397 controls. Participants reported demographic and food frequency information. Blood samples were tested for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg), hepatitis C virus (HCV) antibody, HCV RNA, and the aflatoxin-associated 249ser TP53 mutation.ResultsHBsAg seropositivity was associated with a significant increase in risk of cirrhosis [odds ratio (OR) = 8.0; 95% confidence interval (CI), 4.4–14.7] as was the presence of HBeAg (OR = 10.3; 95% CI, 2.0–53.9) and HCV infection (OR = 3.3; 95% CI, 1.2–9.5). We present novel data that exposure to aflatoxin, as assessed both by high lifetime groundnut (peanut) intake and by the presence of the 249ser TP53 mutation in plasma, is associated with a significant increase in the risk for cirrhosis (OR = 2.8; 95% CI, 1.1–7.7 and OR = 3.8; 95% CI, 1.5–9.6, respectively). Additionally, aflatoxin and hepatitis B virus exposure appeared to interact synergistically to substantially increase the risk of cirrhosis, although this was not statistically significant.ConclusionsOur results suggest that the spectrum of morbidity associated with aflatoxin exposure could include cirrhosis.

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“…The consumption of aflatoxin-contaminated peanut meal was reported to induce different degrees of hepatic lesions including formation of fatty cysts, fibrosis, and cirrhosis among children in a clinical study. 29 In animal studies, administration of aflatoxin or aflatoxin poisoning lead to liver cell damage, [30][31][32] mononuclear cell infiltration, 30,33,34 and periportal fibrosis in the liver. [30][31][32][33][34] The underlying mechanism of aflatoxin-induced cirrhosis remains unclear.…”

Section: Cancer Epidemiologymentioning

confidence: 99%

Aflatoxin B₁ exposure increases the risk of cirrhosis and hepatocellular carcinoma in chronic hepatitis B virus carriers

Chu

Yang

et al. 2017

Intl Journal of Cancer

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The relation between aflatoxin B1 (AFB1) and cirrhosis in chronic carriers of hepatitis B virus (HBV) remains inconclusive. This case-control study nested in a large community-based cohort aimed to assess the effect of AFB1 exposure on cirrhosis and HCC in chronic HBV carriers. Serum AFB1-albumin adduct levels at study entry were measured in 232 cirrhosis cases, 262 HCC cases and 577 controls. Multivariate-adjusted odds ratios (aORs) and 95% confidence intervals (95% CIs) were estimated using logistic regression. Among all chronic HBV carriers, the time intervals between study entry and diagnosis of HCC, cirrhosis, cirrhotic HCC, and non-cirrhotic HCC were all significantly (p<0.0001) shorter in participants with high serum levels of AFB1-albumin adducts than those with low/undetectable levels. There were significant dose-response relations with serum AFB1-albumin adduct level at study entry for cirrhosis (p-trend=0.0001) and cirrhotic HCC (p-trend<0.0001) newly-diagnosed within 9 years after entry as well as non-cirrhotic HCC (p-trend=0.021) newly-diagnosed within 4 years after entry. The aORs (95% CIs) for high vs. undetectable serum AFB1-albumin adduct levels were 2.45 (1.51–3.98) for cirrhosis (p=0.0003), 5.47 (2.20–13.63) for cirrhotic HCC (p=0.0003), and 5.39 (1.11–26.18) for non-cirrhotic (p=0.0368) HCC, respectively. There remained a significant dose-response relation between serum AFB1-albumin adduct level and HCC risk (p-trend=0.0291) in cirrhosis patients, showing an aOR (95% CI) of 3.04 (1.11–8.30) for high vs. undetectable serum levels (p=0.0299). It is concluded that AFB1 exposure may increase the risk of cirrhosis and HCC in a dose-response manner among chronic HBV carriers.

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Experimental induction of liver fibrosis in young guinea pigs by combined application of copper sulphate and aflatoxin B1

Cited by 9 publications

References 25 publications

Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin Exposure and Viral Hepatitis in the Etiology of Liver Cirrhosis in The Gambia, West Africa

Aflatoxin B₁ exposure increases the risk of cirrhosis and hepatocellular carcinoma in chronic hepatitis B virus carriers

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Experimental induction of liver fibrosis in young guinea pigs by combined application of copper sulphate and aflatoxin B1

Cited by 9 publications

References 25 publications

Aflatoxin B1exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin B1exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin Exposure and Viral Hepatitis in the Etiology of Liver Cirrhosis in The Gambia, West Africa

Aflatoxin B1 exposure increases the risk of cirrhosis and hepatocellular carcinoma in chronic hepatitis B virus carriers

Contact Info

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Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin B₁exposure and liver cirrhosis in Guatemala: a case–control study

Aflatoxin B₁ exposure increases the risk of cirrhosis and hepatocellular carcinoma in chronic hepatitis B virus carriers