**1. Introduction**

Mycotoxins are secondary metabolic products produced by moulds common in the food chain, causing major economic losses and becoming also sources of public health threats. These mycotoxins have a number of adverse health effects in humans and animals. They can be carcinogenic, immune-damaging, teratogenic, neurotoxic, kidney and liver-damaging depending on the species, age, and sex of the consumer. A mould can produce a variety of mycotoxins, and these compounds can amplify the harmful effects of each other. Due to global climate change, mould strains so far only causing problems with their mycotoxin production in the tropical climate zone have also appeared in Hungary [1]. Some 300 compounds have been recognised as mycotoxins of which around thirty are considered as a threat to human or animal health [2].

An example of a mycotoxin producing mould is *Aspergillus flavus*, a species of several strains able to produce mycotoxins. By infecting fodder plants like corn, wheat, and oily seeds as for example peanuts and walnuts, the mycotoxin formed enters the food chain [3]. The four most important aflatoxins produced by *A. flavus* are AFB1, AFB2, AFG1, and AFG2 [4].

Aflatoxin B1 (AFB1) is one of the most dangerous mycotoxins, primarily carcinogenic and genotoxic, harmful to the liver. The IARC classifies AFB1 in Group 1 (Carcinogenic to humans). It is a relatively heat-stable compound, up to 250 ◦C it is unchanged in roasted nuts, but in aqueous environments, it almost completely decomposes at 160 ◦C [5]. In accordance with Regulation (EU) No 574/2011, the maximum permitted level for AFB1 in feed is 0.02 mg/kg [6].

Sterigmatocystin (ST) is a precursor of aflatoxin. It is also produced by fungal species like *A. flavus*, *A. parasiticus*, *A. versicolor*, and *A. nidulans*. *A. flavus* and *A. parasiticus* are able to convert ST into aflatoxin, while *A. versicolor* and *A. nidulans* are not capable of this, resulting in elevated levels of ST in crops infected by them [7,8]. Rice and oats are typically the most contaminated with ST [9]. It is possible to reduce the level of ST by roasting [10]. Although experiments have shown genotoxicity and carcinogenicity of ST, limited data are available on the tumorigenic effect of the mycotoxin, which is why IARC has classified it as a potential human carcinogen (Group 2B).

Co-occurrence of aflatoxin and sterigmatocystin is recently gaining attention, as researches are being conducted and published on the sterigmatocystin contaminations as well for example in wheat and wheat products in the supermarkets in China [11] or corn, soybean meal, and formula feed in Japan [12].

Physical, chemical, and biological methods exist to prevent mycotoxins from entering the food chain. Microbes are used in biological detoxification. They may be capable of either inhibiting the growth of mycotoxin-producing fungi or of binding the mycotoxin to their surface, or, in rare cases, of degrading the mycotoxin itself [13]. The most detailed model of microbial mycotoxin binding has been described for zearalenone binding of *Saccharomyces* spp. In the adsorption of the mycotoxin, the beta-1,3/1,6-glucan moieties play a crucial role [14]. For AFB1-binding, glucomannans and mannanoligosaccharides have been proposed to be responsible for yeast cell walls. Similar to yeast, polysaccharides have been proposed to be the most crucial elements responsible for AFB1 binding in lactic acid bacteria (LAB) [15]. These polysaccharides are present in three main forms in the cell wall of lactobacilli: exopolysaccharides (EPS), peptidoglycan, and teichoic or lipoteichoic acids [16,17]. Lahtinen et al. [18] reported the ability of peptidoglucan to bind AFB1 in *L. rhamnosus*, and stated that the other glucan fractions, like EPS, lacked the mycotoxin-binding ability. However, the prominent role of peptidoglycan in binding is questionable, because, in 2010, Chapot-Chartier et al. described a new non-EPS cell wall polysaccharide, WPS, in *L. lactis*, which covalently binds to peptidoglycan forming a layer over it [19]. WPS appear as omnipresent components of the cell surface of LAB and exhibit most probably high structural diversity between strains even belonging to the same species.

Lactic acid bacteria (LAB) are found in both the animal and the human body. They got their name from the fact that glucose is fermented into lactic acid by them. They are Gram-positive, non-sporulating, oxidase and catalase-negative, anaerobic aerotolerant microorganisms. The most important genera belonging here are *Lactobacillus, Lactococcus, Leuconostoc, Enterococcus* and *Pediococcus*. Three hundred and three known species belong to the genus *Lactobacillus*, 17 species to the genus *Lactococcus*, 69 species to the genus *Enterococcus*, 15 species to the genus *Pediococcus*, and 27 species to the genus *Leuconostoc*.

As a member of the gut microbiota, they inhibit the growth of harmful microbes. Furthermore, they produce vitamins (e.g., vitamin B1, vitamin B2, vitamin B12, and vitamin K) [20] and stimulate the immune system [21]. In addition, numerous studies have shown that certain strains of some LAB species can bind mycotoxins, for example, AFB1, to their surface [22–24].

At our department, microbes with colony morphology of lactic acid bacteria were isolated on LAB selective MRS (de Man, Rogosa and Sharpe) plates from 14 exotic animals of the Budapest Zoo and Botanical Garden. The molecular taxonomical identification of the strains was carried out by 16S rDNA sequencing and analysis. At present, the collection comprises nearly 1000 strains and is constantly expanding. Most of our strains belong to the genera *Lactobacillus* and *Enterococcus*, but we also managed to isolate strains belonging to the other LAB genera.

Our goal was to screen strains of the genus *Lactobacillus* from our collection for AFB1 and ST binding capacities. For this purpose, a rapid high-performance liquid chromatography method was developed and used for analytical determination of AFB1 and ST in both the bacterial biomass and its supernatant.
