Impact of DON and BEA on oocyte development
In a recent cooperation with Utrecht University (NL), the reproductive impact of DON and BEA on gilts and sows was evaluated with remarkable results. This article summarises the main findings of the study .
BY REGIANE SANTOS, INDEPENDENT CORRESPONDENT D
60 75
15 30 45
0 Control 0.02 0.2 2.0
eoxynivalenol (DON) and beauvericin (BEA) are toxins produced by the Fusarium species that can contaminate food and feed. The negative impact caused by DON in pigs is well known, and studies
also indicate that pigs are sensitive to BEA. In Europe, it is recommended that pig diets do not contain more than 900 ppb DON, regardless of the age of the animal; however, there is no recommendation regarding the maximum dietary levels of BEA.
Redox balance in gilts and sows Besides being toxic to the intestinal tract, both DON and BEA can impair the reproduction of female pigs, specifically by causing damage in their gametes, which are also called oo- cytes. These reproductive cells are constantly maintaining a balance between the production of reactive oxygen species (ROS) and their antioxidant activity to guarantee a healthy re- productive system. At an advanced stage of development, these oocytes are enclosed as a follicle and are surrounded by
Figure 1 - Mean rates of oocyte maturation and degeneration of porcine in vitro matured in the absence (control) or in the presence of DON at different concentrations (0.02, 0.2 or 2.0 µmol/L).
d d c c Gilt Sow b b b a
Beauvericin’s effect on gilt oocytes A significant decrease in the rate of oocyte maturation was observed in gilt oocytes already in the presence of 0.5 µmol/L
28 ▶ MYCOTOXINS | NOVEMBER 2021
somatic cells (cumulus cells) and a follicular fluid (FF) pro- duced by somatic cells. The communication of these com- partments via endocrine signals and redox balance maintain oocyte quality for further fertilisation. In pre-pubertal gilts, the endocrine signals to initiate puberty allow a growth of follicles of up to approximately 6 mm but do not support their final development. Thus, the first oestrus of gilts is clas- sified as a heat-no-serve. This is likely an additional result of a not yet efficient redox balance. Based on this information, we hypothesise that oocytes from gilts and sows will respond differently to DON and BEA exposure during in vitro maturation and that the follicular redox system plays an important role in these differences. To assess this hypothesis, we evaluated the effect of DON and BEA at different concentrations on in vitro maturation of oocytes from gilts and sows. Furthermore, anti- oxidant levels in the oocytes and cumulus cells, as well as the relative mRNA expression of redox markers, were established.
In vitro oocytes maturation As confirmed by mRNA expression analysis, in vitro matured oocytes from gilts had a lower expression of superoxide dis- mutase 1 (SOD1) and glutathione synthetase (GSS) than sows. This indicates that oocytes from sows are more active in neutralising superoxide anions in the cytoplasm of these fe- male gametes and that the GSS supports further develop- ment of embryos. Oocytes and their surrounding cumulus cells from gilts and sows were evaluated before and after in vitro maturation in the absence or presence of DON (0.02, 0.2 or 2.0 µmol/L) or BEA (0.5, 2.5 or 5.0 µmol/L). The results are detailed in Figures 1 and 2.
Presence of DON Regardless of age (gilts or sows), a significant decrease in the rate of oocyte maturation was observed when oocytes were in vitro matured in the presence of 0.02 or 0.2 µmol/L DON, and this negative impact was even more prominent at a con- centration of 2.0 µmol/L. In addition, gilt oocytes were more sensitive to DON exposure than sow oocytes. The degenera- tion rate ranged from 8.8% to 35.4%, but no effect on DON exposure was observed (Figure 1).
% maturation
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80
