Compound	Half‐life				Stability
	Study	Animals	Treatment details	Time
OTA	Hagelberg et al. (1989) a	Wistar rats	Oral or i.v. administration of 50 µg/kg bw	Plasma: 5 days
	Hult et al. (1979) b	Pigs	i.v. administration of 50 µg of toxin per kg bw	Plasma: 6 days
	Stander et al. (2001)	Monkeys	i.v. injection, 0,8, 1,5 and 2 mg/kg bw	Plasma: 19–21 days, average total body clearance 0.22 mL/h per kg bw
	Han et al. (2013)	Male SD rats	gavage of a single dose of 0.2 mg OTA/kg bw	Plasma: 76 h (± 3 days)
	Studer‐Rohr et al. (2000)	A male adult volunteer (empty stomach)	Single oral dose (0.02 nmol/kg bw) of tritium‐labelled OTA	First 6 days: about 20 h After 6 days: 35 days
	Mantle (2008)	Rats (Fischer, F1 hybrids from SD and Fisher Dark Agouti)	gavage or via feed. Doses ranging from 50 to 30,000 µg/kg bw	Fischer rats: 8–10 days Dark Agouti rats: 2–3 days
Chloramphenicol	Nouws and Ziv (1978)	Dairy cows	Single i.m. dose of 43 mg/kg bw	Muscle: 14 h Kidney: 22 h
	Nouws and Ziv (1979)	Cows, sheep and goat	i.m. injections, 36 and 50 mg/kg bw	Blood: 88–643 min, depending on the preparation and plasma levels
	Nouws and Ziv (1982)	Dairy cows	Intramammary infusion 5, 12.5, 25 g	Serum levels: 146, 213 and 285 min
	Nouws et al. (1986)	Dairy cows and ruminant calves	Single i.m. injection, 50 mg/kg bw	Plasma and milk: 10 h
	Burrows et al. (1984)	Calves	25 mg/kg bw	Plasma:450 min to 3 days and 150 min, depending on age
	Sanders et al. (1988)	Bullocks	i.v. injection 40 mg/kg bw and after two weeks either i.m. or s.c. treatment with 90 mg/kg, which was repeated after 48h. same treatment after another 3 weeks	Plasma: 4 h
	Gassner and Wuethrich (1994)	Female beef‐type calves	4 oral doses, 25 mg/kg bw at 12 h intervals	Plasma: 4.5 h
	Etuk and Onyeyili (2005a, 2005b)	Sokoto red goats	Single i.v. dose of 25 g/kg bw	Plasma: 0.13–3.6 h Tissues (liver, kidney, lung, heart, spleen and bone marrow): 1–4 h Tissues (muscle and brain): 24 and 21 h, respectively. Levels in muscle were not detectable after 11 days
	Dagorn et al. (1990)	Sheep	i.v., i.m. or s.c. single dose of 30 mg/kg bw	Plasma: 1.7 (i.v.), 2.7 (i.m.) and 17.9 h (s.c.)
	Rao and Clarenburg (1977)	7‐week‐old pigs	i.v. administration of 22 mg/kg bw	Plasma: 55 min
	Mercer et al. (1978)	12‐ to 16‐week old crossbred pigs	i.v. administration of 22 mg/kg bw	Plasma: 2.6 ± 1 h Kidney: 1.25 h Fat: 5.89 h Most major organs: 2–5 h
	Buonpane et al. (1988)	Foals	oral administration of 50 mg/kg bw	Serum: 1.44 h
	Gronwall et al. (1986)	Adult horses	Intragastrical administration of 50 mg/kg bw	Serum: 1.8 h
Nitrofurans	Cooper et al. (2005)	8‐week‐old‐piglets	Fed for 10 days with feed medicated with furazolidone, furaltadone, nitrofurantoin or nitrofurazone at a dose of 400 mg/kg feed	No parent compounds could be detected AOZ (in the case of furazolidone): Liver and kidney: 7 days Muscle: 12 days AHD (in the case of nitrofurantoin): Muscle: 15 days	Cooper and Kennedy ( 2007 ): storage of pig liver and muscle at −20°C for 8 months did not cause a significant reduction of the concentrations of marker metabolites (AOZ, AMOZ, AHD and SEM)
	Nouws and Laurensen (1990) and McCracken et al. (1995)	Nitrofuran parent compounds have a short in vivo half‐life due to extensive metabolism, primarily a reduction of the nitro‐group, such that they do not occur generally as residues in foods of animal origin. Therefore, monitoring of nitrofuran residues in livestock based on the identification of the parent compounds is not appropriate
	Vroomen Louis et al. (1986), Hoogenboom et al. (1991, 1992) and Vass et al. (2008)	The nitro reduction results in the formation of reactive metabolites able to bind covalently to tissue macromolecules, including proteins, which, in food‐producing animals, have relatively long half‐lives, persisting for several weeks in edible tissues
	Hoogenboom et al. (1991), Hoogenboom and Polman (1993), Horne et al. (1996) and Leitner et al. (2001)	As nitrofuran parent compounds do not persist as residues in animal tissues and do not occur at concentrations comparable to those of the marker metabolites (as protein‐bound adducts), the marker metabolites AOZ, AMOZ, AHD, SEM and DNSH are appropriate for identifying the illicit use of nitrofurans
Compound	Study	Animals	Treatment details		Residues found in tissues (ng/g)
Zeranol	Jansky (1983) in Paris et al. (2006)	Male calves	Témoins, 1 à 3 implantations of Ralgo® (1 to 3 × 65 days) 6 implantations of Ralgo® (6 × 65 days)		Liver: 0.102; 0.315; 1.209 Kidney: 0.014; 0.104; 0.219 Muscle: 0.105; 0.040; 0.115 Adipose tissue: 0.010; 0.039; 0.218
	O'Keeffe (1984) in Paris et al. (2006)	Steers	Témoins, Ralgo®		Liver: 0.140; 0.350 Kidney: 0.028; 0.076 Muscle: 0.001; 0.014 Adipose tissue: 0.064; 0.060
	Dixon and Russell (1986) in Paris et al. (2006)	Cows	Ralgo® (70 days after implantation)		Liver: 0.300 Kidney: 0.160 Muscle: 0.130 Adipose tissue: 0.180
	Dixon et al. (1986) in Paris et al. (2006)	Steers	Témoins Ralgo® (7 days after implantation) Ralgo® (30 days after implantation) Ralgo® (70 days after implantation) Ralgo® (120 days after implantation)		Liver: 0.100; 0.470; 0.810; 0.200; 0.100 Kidney: 0.100; no result; no result; 0.130; 0.084 Muscle: 0.280; 0.290; 0.280; 0.730; 0.280 Adipose tissue: 0.075; 0.077; 0.110; 0.073; 0.066
	Paris et al. (2006)	Residues of zeranol and trenbolone do not occur in animal tissues under normal conditions but can be measured following the use of GPHs containing these compounds. It should be noted that the mycotoxin zearalenone can be present in various feed materials can be converted into zeranol. This fact might complicate the monitoring of undesirable residues in animal tissues
	Gajecka (2013)	In prepubertal female beagle dogs, orally administered with ZEN for 42 days, the presence of ZEN and α‐ and β‐ZEL was observed in plasma throughout the experiment. The highest relative α‐ZEL concentration (58–74% of ZEN) was observed on the last 5 days in the high‐dose group
	EFSA CONTAM Panel (2011c)	Limited data on food of animal origin did not show ZEN or its phase I metabolites above the detection limits. This led the CONTAM Panel to state that it seemed reasonable to conclude that the possible contribution of ZEN residues in animal products is negligible for the total ZEN exposure of the consumer

AHD: 1‐aminohydantoin, AMOZ: 3‐amino‐5‐methylmorpholino‐2‐oxazolidinone; AOZ: 3‐amino‐2‐oxazolidinone; DNSH: 3,5‐dinitrosalicylic acid hydrazide; i.m.: intramuscular, i.v.: intravenous, OTA: ochratoxin A; SD: Sprague Dawley; s.c.: subcutaneous; SEM: semicarbazide; ZEN: zearalenone; α‐ZEL: α‐zearalenol; β‐ZEL: β‐zearalenol.

^aEFSA (2006) stated that the data is mentioned in Dietrich et al, 2005, but the original data and study design is found in Hagelberg et al. (1989).

^bEFSA (2006) stated that the data is mentioned in Dietrich et al, 2005, but the original data and study design is found in Hult et al. (1979).