Introduction
The toxicokinetics of mycotoxins comprise the processes of absorption, distribution, metabolism and excretion (ADME), encompassing all stages from the entry of the toxin into the organism, through its biotransformation, to its final elimination via excretion. These processes vary according to the type of mycotoxin and the animal species exposed. In swine, their effects also vary across different production stages.
In addition, the concept of carry-over refers to the transfer of mycotoxins from contaminated feed consumed by livestock to food products of animal origin intended for human consumption, thereby posing a risk to public health.
Aflatoxins
Aflatoxins are primarily absorbed in the intestine, specifically in the duodenum. They are a family of low-molecular-weight, lipophilic mycotoxins, characteristics that contribute to efficient oral absorption, with rates reaching approximately 90% (Schrenk et al., 2020a).
Aflatoxins are widely distributed throughout the body, reaching the digestive tract, liver and kidneys. The liver is the primary target organ, and prolonged exposure may lead to lesions such as hepatocellular carcinoma (Schrenk et al., 2020a).
Aflatoxins are metabolised in the liver, giving rise to several metabolites, among which AFB1-8,9-epoxide (AFBO) is particularly noteworthy. This metabolite of aflatoxin B1 is formed via cytochrome P450 and is more toxic than the parent compound. Other products of aflatoxin biotransformation include AFM1, AFQ1 and aflatoxicol (Coppock et al., 2018).
Swine have a limited capacity to detoxify and excrete aflatoxins, which increases their susceptibility to aflatoxicosis. Elimination occurs mainly via the biliary route and, to a lesser extent, via the urinary route, and proceeds slowly. Approximately 20% of these compounds are excreted in urine within nine days of exposure (Popescu et al., 2022).
Aflatoxins exhibit carry-over, as they have been detected in meat and milk; both the parent compounds and their metabolites may enter the human food chain and be transferred to piglets during lactation (Popescu et al., 2022; Lee et al., 2017).
Deoxynivalenol
In pigs, deoxynivalenol (DON) is rapidly absorbed following ingestion of contaminated feed, typically within 1 to 3 hours (Sun et al., 2022). The extent of absorption varies with the production stage; however, DON generally shows high bioavailability in swine (50%-100%) (Schelstraete et al., 2020; Dänicke et al., 2013).
DON is rapidly and widely distributed, reaching blood, muscle, abdominal fat, stomach, intestine, liver, kidneys, heart, brain, lungs, skin, spleen, testes, ovaries and adrenal glands (Lin et al., 2025). However, tissue exposure is transient, as DON does not accumulate in these tissues (Dersjant-Li et al., 2003).
DON is metabolised via two main pathways: conjugation and de-epoxidation. In swine, conjugation with glucuronic acid is the predominant pathway, giving rise to metabolites such as DON-3-GlcA and DON-15-GlcA. De-epoxidation of DON leads to the formation of DOM-1; however, this process is variable, as some pigs lack the de-epoxidising intestinal microbiota required (Sun et al., 2022).
Urinary excretion accounts for 90-95% of DON elimination in pigs (Dänicke et al., 2013), while less than 5% of DON and its metabolites is excreted via the faeces (Schelstraete et al., 2020). The elimination half-life ranges from 1.5 to 5 hours, which is relatively prolonged and contributes to the susceptibility of swine to this mycotoxin (Sun et al., 2022).
Despite the high systemic bioavailability of DON in swine, its carry-over into tissues such as muscle and fat remains poorly characterised (Schelstraete et al., 2020; Dänicke et al., 2013). However, as observed for aflatoxins, both DON and its metabolites have been detected in the colostrum and milk of lactating sows (Benthem de Grave et al., 2021). In addition, placental transfer of these compounds to piglets during gestation has been reported (Sayyari et al., 2018; Dänicke et al., 2007).
Zearalenone
The absorption rate of zearalenone (ZEN) in pigs has been estimated at 80-85%, although its bioavailability may be lower in younger animals (Liu et al., 2020; Catteuw et al., 2019). Absorption is rapid, and ZEN and its metabolites can be detected in plasma as early as 30 minutes after ingestion of contaminated feed (Lin et al., 2025).
Following absorption, ZEN and its metabolites are widely distributed and can be detected in the liver, bile, plasma, urine, and faeces (Liu et al., 2020). The reproductive tract is the primary target system affected by this mycotoxin, with females being the most susceptible group (Rai et al., 2020).
In pigs, the main metabolites are glucuronide conjugates of ZEN and α-zearalenol (α-ZEL), the latter being the predominant form (Liu et al., 2020). This metabolite shows a higher affinity for oestrogen receptors than other metabolites, which accounts for the high sensitivity of swine to the pathological effects of ZEN (Schelstraete et al., 2020).
The urinary tract is the primary route of excretion of this mycotoxin in pigs, with approximately twice as much being excreted in urine than in faeces (Liu et al., 2020). Following oral exposure to ZEN, between 14% and 45% is detected in urine, both as the parent compound and as metabolites (Schelstraete et al., 2020). The elimination half-life of this mycotoxin in pigs is highly variable, with reported values ranging from 2.63 and 86.6 hours (Catteuw et al., 2019).
Carry-over of this mycotoxin into meat and milk has been reported in swine. Both ZEN and its metabolites have been detected in muscle and various organs, posing a risk to public health. Transfer to piglets during the lactation period has also been documented (Benthem de Grave et al., 2021; Liu et al., 2020).
Ochratoxin A
Ochratoxin A (OTA) is rapidly absorbed and exhibits high bioavailability in pigs, with values of up to 66% reported (Tolosa et al., 2021). Within a few hours of ingestion, it can be detected in the blood, from where it is distributed via the portal circulation (Schrenk et al., 2020b; Ringot et al., 2006).
In swine, OTA is widely distributed, reaching the liver, kidneys, muscle, and fat. It shows a high affinity for plasma proteins, particularly albumin; only around 0.1% remains unbound after entering the organism (Ringot et al., 2006). This, together with its slow metabolism, results in a prolonged half-life (Hagelberg et al., 1989).
The main metabolite of OTA in swine is OTα, which is produced by the intestinal microbiota. The principal metabolic pathway involves hydrolysis to OTα followed by conjugation with glucuronic acid. This metabolite is partially absorbed in the intestine and rapidly excreted in urine, as it does not accumulate in renal tissue (Schrenk et al., 2020b).
However, the excretion of OTA is complex; it is eliminated slowly via the urinary route over periods exceeding five days (Schrenk et al., 2020b). OTA accumulates in renal tissue, and pigs are among the species most sensitive to its nephrotoxic effects (EFSA, 2006).
OTA exhibits carry-over in various tissues and has been detected in a range of pork-derived products (Ganesan et al., 2022; Tolosa et al., 2021). Furthermore, it can be transferred to the foetus during gestation via the placenta (Ringot et al., 2006).
Fumonisins
Fumonisins exhibit low absorption in swine, ranging from 3% to 5% (Knutsen et al., 2018; Prelusky et al., 1994). Within 30-40 minutes of oral exposure, these compounds can be detected in the blood, reaching peak concentrations after 60 to 90 minutes (Schertz et al., 2018).
These mycotoxins are rapidly distributed to various tissues, including the intestine, liver, pancreas and kidneys, and have a blood half-life of less than 4 hours (Knutsen, et al., 2018). In addition, they alter the sphinganine/sphingosine (Sa/So) ratio due to their structural similarity to endogenous compounds, particularly ceramide synthase (Schertz et al., 2018).
In mammals, fumonisin B1 is metabolised via a single metabolic pathway involving hydrolysis of its side chains, giving rise to metabolites such as HFB and pHFB (Schelstraete et al., 2020; Knutsen et al., 2018). Consequently, fumonisins are only minimally metabolised (Schertz et al., 2018).
A large proportion of fumonisins are eliminated via biliary excretion without prior biotransformation. Excretion occurs primarily through the faeces (up to 90%) and, to a very limited extent, via the urinary route. This process is relatively slow (Knutsen et al., 2018).
Carry-over of this group of mycotoxins has been detected in various tissues following prolonged exposure to contaminated diets (Dersjant-Li et al., 2003). In addition, there is evidence of the transfer of fumonisin B1 into the milk of exposed sows and, consequently, to piglets (Zomborszky-Kovács et al., 2000).
T-2 Toxin
T-2 toxin is rapidly absorbed via both oral and inhalation routes (Schuhmacher et al., 2010); however, its oral bioavailability is very low (Sokolović et al., 2008).
Both T-2 toxin and its metabolites are rapidly and widely distributed throughout the body, primarily to the liver, kidneys and small intestine. They also distribute to other tissues, such as adipose tissue, where they exhibit a longer elimination half-life (Yong-xue et al., 2012).
T-2 toxin is rapidly metabolised, yielding a wide range of metabolites, most notably HT-2, which is formed through hydrolysis (CONTAM, 2011).
T-2 toxin and its metabolites are rapidly eliminated via the urinary route, while only a minor proportion is excreted via the faeces (Yong-xue et al., 2012; Schuhmacher et al., 2010). In this context, the study of distribution and elimination is complex due to rapid excretion (Schuhmacher et al., 2010). An average elimination time of approximately 90 minutes has been reported (CONTAM, 2011).
With regard to carry-over, this mycotoxin has not been detected in products within the food chain to date. This is because neither T-2 toxin nor its metabolites show significant accumulation in tissues (Kalantari et al., 2010; Schuhmacher et al., 2010).
Conclusion
In recent years, the number of studies on the toxicokinetics of mycotoxins has progressively increased, providing essential information for understanding their passage through the organism of animals, and, therefore, their harmful effects on animal production. However, there are still many aspects about which we must continue to research, in order to understand the action of these substances in pigs, and to be able to implement effective strategies for their mitigation.
