Ovarian consequences of low dose peroral Fusarium (T-2) toxin in a ewe and heifer model.
The effect of low dose peroral Fusarium produced T-2 toxin intake upon the ovarian function was evaluated in ewes (n = 30; Trial 1) and heifers (n = 7; Trial 2). Half of the ewes and all of the heifers were fed rich, acidosis-inducing concentrate. The 30 ewes were divided into 6 groups of 5 animals each. They were given 0, 0.3 or 0.9 mg/day (0, 5 or 15 ug/kg) purified T-2 toxin per os for 21 days (3x2 factorial design). Four of the 7 heifers were fed 9 mg/day (25 ug/kg) of the same purified T-2 toxin for 20 days while 3 remained untreated. The estrus cycles in all animals were synchronized prior to the trials and the T-2 exposure was started in the mid-luteal phase. The acidic condition in the rumen was estimated by the determination of urinary net acid-base excretion. The ovarian activity was followed with blood sampling for progesterone on alternate days (Trial 1) or with ultrasonography and sampling for progesterone daily (Trial 2). All of the heifers and concentrate-fed ewes showed a compensated acidosis, during first two thirds of T-2 exposure. In Trial 1, ovarian malfunction manifested as lower P4 peak concentration in the midluteal phase, shortening of the CL lifespan and prolonged follicular phases. These malfunctions were detected in 3 and 3 ewes fed concentrate and 0.3 mg and 0.9 mg T-2 toxin. Lower P4 peak concentration was observed in 1 ewe fed regular diet and 0.9 mg T-2 toxin. None of the control and acidotic groups (0 mg T-2), or ewes fed regular diet with 0.3 mg T-2 showed any ovarian malfunction. In Trial 2, after PGF2, administration the ovulation occured later and the plasma progesterone level remained low (< 3 nmol/l) for a longer period in T-2 treated heifers, than their untreated control mates (5.0+/-0.7 vs 3.7+/-0.5 d, P<0.05 and 8.3+/-0.4 vs 6.3+/-0.9 d, P<0.01, respectively). These results show that the peroral T-2 intake can significantly retard the folliculus maturation and ovulation and perhaps the subsequent luteinisation also in ruminants kept on concentrate-rich diet.
Huszenicza
G
G
Faculty of Veterinary Science, Szent Istvan University, Budapest, Hungary.
Fekete
S
S
Szigeti
G
G
Kulcsár
M
M
Fébel
H
H
Kellems
R O
RO
Nagy
P
P
Cseh
S
S
Veresegyházy
T
T
Hullár
I
I
D000138:Acidosis / Q000209:etiology / Q000503:physiopathology / Q000662:veterinary; D000284:Administration, Oral; D000821:Animal Feed / Q000009:adverse effects; D000818:Animals; D002417:Cattle / Q000502:physiology*; D015237:Dinoprost / Q000008:administration & dosage / Q000502:physiology; D004973:Estrus Synchronization; D005260:Female; D003425:Flurogestone Acetate / Q000008:administration & dosage; D010053:Ovary / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000502:physiology; D011374:Progesterone / Q000097:blood; D045167:Progesterone Congeners / Q000008:administration & dosage; D011863:Radioimmunoassay / Q000662:veterinary; D011897:Random Allocation; D012756:Sheep / Q000502:physiology*; D013605:T-2 Toxin / Q000008:administration & dosage / Q000633:toxicity*; D014463:Ultrasonography
D045167:Progesterone Congeners; D011374:Progesterone; D015237:Dinoprost; D013605:T-2 Toxin; D003425:Flurogestone Acetate