Ochratoxin A (OTA) is a ubiquitous mycotoxin produced by fungi of improperly stored food products. OTA is nephrotoxic and is suspected of being the main etiological agent responsible for human Balkan endemic nephropathy (BEN) and associated urinary tract tumours. Striking similarities between OTA-induced porcine nephropathy in pigs and BEN in humans are observed. International Agency for Research on Cancer (IARC) has classified OTA as a possible human carcinogen (group 2B). Currently, the mode of carcinogenic action by OTA is unknown. OTA is genotoxic following oxidative metabolism. This activity is thought to play a central role in OTA-mediated carcinogenesis and may be divided into direct (covalent DNA adduction) and indirect (oxidative DNA damage) mechanisms of action. Evidence for a direct mode of genotoxicity has been derived from the sensitive 32P-postlabelling assay. OTA facilitates guanine-specific DNA adducts in vitro and in rat and pig kidney orally dosed, one adduct comigrates with a synthetic carbon (C)-bonded C8-dG OTA adduct standard. In this paper, our current understanding of OTA toxicity and carcinogenicity are reviewed. The available evidence suggests that OTA is a genotoxic carcinogen by induction of oxidative DNA lesions coupled with direct DNA adducts via quinone formation. This mechanism of action should be used to establish acceptable intake levels of OTA from human food sources.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mnfr.200790020

Ochratoxin A: An overview on toxicity and carcinogenicity in animals and humans

Aflatoxins, fungal toxins produced by Aspergillus flavus and Aspergillus parasiticus in a variety of food crops, are well known as potent human hepatocarcinogens. Relatively less highlighted in the literature is the association between aflatoxin and growth impairment in children. Foodborne aflatoxin exposure, especially through maize and groundnuts, is common in much of Africa and Asia—areas where childhood stunting and underweight are also common, due to a variety of possibly interacting factors such as enteric diseases, socioeconomic status, and suboptimal nutrition. The effects of aflatoxin on growth impairment in animals and human children are reviewed, including studies that assess aflatoxin exposure in utero and through breastfeeding. Childhood weaning diets in various regions of the world are briefly discussed. This review suggests that aflatoxin exposure and its association with growth impairment in children could contribute a significant public health burden in less developed countries.

Aflatoxins and growth impairment: A review

Since ochratoxin A (OTA) was discovered, it has been ubiquitous as a natural contaminant of moldy food and feed. The multiple toxic effects of OTA are a real threat for human beings and animal health. For example, OTA can cause porcine nephropathy but can also damage poultries. Humans exposed to OTA can develop (notably by inhalation in the development of acute renal failure within 24 h) a range of chronic disorders such as upper urothelial carcinoma. OTA plays the main role in the pathogenesis of some renal diseases including Balkan endemic nephropathy, kidney tumors occurring in certain endemic regions of the Balkan Peninsula, and chronic interstitial nephropathy occurring in Northern African countries and likely in other parts of the world. OTA leads to DNA adduct formation, which is known for its genotoxicity and carcinogenicity. The present article discusses how renal carcinogenicity and nephrotoxicity cause both oxidative stress and direct genotoxicity. Careful analyses of the data show that OTA carcinogenic effects are due to combined direct and indirect mechanisms (e.g., genotoxicity, oxidative stress, epigenetic factors). Altogether this provides strong evidence that OTA carcinogenicity can also occur in humans.

https://www.mdpi.com/2072-6651/8/7/191/pdf

Ochratoxin A: 50 Years of Research

Liver cancer is the most common malignancy of the digestive system with high death rate. Accumulating evidences suggests that many dietary natural products are potential sources for prevention and treatment of liver cancer, such as grapes, black currant, plum, pomegranate, cruciferous vegetables, French beans, tomatoes, asparagus, garlic, turmeric, ginger, soy, rice bran, and some edible macro-fungi. These dietary natural products and their active components could affect the development and progression of liver cancer in various ways, such as inhibiting tumor cell growth and metastasis, protecting against liver carcinogens, immunomodulating and enhancing effects of chemotherapeutic drugs. This review summarizes the potential prevention and treatment activities of dietary natural products and their major bioactive constituents on liver cancer, and discusses possible mechanisms of action.

https://www.mdpi.com/2072-6643/8/3/156/pdf

Dietary Natural Products for Prevention and Treatment of Liver Cancer

Molecules of InterestCarnosic acid

Since oxidative stress plays an important role in the toxicity mechanism of several mycotoxins such as aflatoxin B1 (AFB1), the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. Carnosic acid (CA) is the major polyphenolic compound present in rosemary plants and it can also be found in sage leaves. Its free radical scavenging properties were tested with two chemical methods. It was found that it has good free radical scavenging capacity at pH 7.4. This study also found that a 24 h pre-treatment with 10, 20 and 30 microm CA led to a clear, dose-dependent protective effect on cell toxicity, reducing cell death induced by a 24 h exposure with 10 microm AFB1, respectively, by 16% (P < 0.05), 26% (P < 0.01) and 63% (P < 0.001). It was also found that a 24 h pre-treatment with 20 and 30 microm CA achieved a reduction of ROS levels, respectively, of 146% (P < 0.001) and 173% (P < 0.001) in HepG2 cells exposed to 10 microm AFB1 for 8 h. Moreover, in cells pre-incubated with 30 microm CA for 24 h the concentration of 8-OH-deoxyguanine decreased by 57% (P < 0.001) with respect to the cells exposed for 24 h to 10 microm AFB1 alone. The results obtained with the in vitro and chemical studies support the theory that AFB1 induced oxidative stress plays an important role in the cytotoxic mechanism of this mycotoxin. Furthermore these findings suggest a starting point for developing alimentary strategies in order to counteract the damage caused by AFB1 contamination in feed and food.

Carnosic acid from rosemary extracts: a potential chemoprotective agent against aflatoxin B1. An in vitro study

Fate of aflatoxin M1 during production and storage of parmesan cheese

SummaryBackground
Many
human milk benefits have been
well documented; nevertheless the
newborn potential risk to the xenobiotic
exposition may be relevant
and it requires a biological monitoring
in general prevention. Concerning
this problem, attention
should be paid to mycotoxins and
heavy metals.Aim of the studyAssessing
the presence of the xenobiotics
aflatoxins, ochratoxin A, lead
and cadmium in human milk,
defining their level of contamination
and evaluate the potential risk
for the newborn derived from this
xenobiotic ingestion.MethodsA
study has been carried out on lactating
women randomly selected in
seven hospitals in Lombardy
(Northern Italy). Two hundred and
forty–seven puerparae were recruited;
231 women participated in
the study. Women’s milk samples
on the third or fourth day after delivery
were tested to determine
aflatoxins and ochratoxin A levels.
Lead and cadmium were determined
in 143 women because supplemental
milk could be taken only
from these women.ResultsAflatoxin
B1 (11.4 ng/l) and aflatoxin
M1 (194 ng/l) were found only in
one sample,while ochratoxin A was
detected in 198 samples (85.7 %) at
an average value of 6.01 ± 8.31 ng/l.
A total of 75.7% of samples were
positive for lead; the cadmium situation
was better with 87.4% of the
sample with values below detection
limits (2 µg/l). A high percentage of
babies (71 %) are exposed to mycotoxin
levels on day 6 greater than
the TDI value of 0.2 ng/kg b.w.
Lead and cadmium presence in human
milk presented risk respectively
for 8% and 0.7% of newborns
on the fourth day; 9.5% and
1.4% on the sixth day.ConclusionsThe study points out that mycotoxins
and lead are present in maternal
milk, and the data confirm the
need to continue biological monitoring
in general prevention.

Evaluation of xenobiotics in human milk and ingestion by the newborn An epidemiological survey in Lombardy

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Carnosic acid from rosemary extracts: a potential chemoprotective agent against aflatoxin B1. An in vitro study

Fate of aflatoxin M1 during production and storage of parmesan cheese

Evaluation of xenobiotics in human milk and ingestion by the newborn An epidemiological survey in Lombardy