Growth and metabolism of Oenococcus oeni for malolactic fermentation under pressure.

Malolactic fermentation is a biological deacidification process of wine, characterized by the transformation of l-malic acid to l-lactic acid and CO2 . Oenococcus oeni is able to perform malolactic fermentation and to survive under wine harsh conditions, representing great interest for wine industry. The aim of this work was to evaluate the effect of high pressure on the metabolism of O. oeni growing in culture media, regarding malolactic fermentation, sugars metabolism and bacterial growth. A pressure stress of 50 MPa during 8 h did not result in significant modifications in bacterial metabolism. In contrast, a stress of 100 MPa during 8 h resulted in lower amounts of l-lactic acid, while higher amounts of d-lactic acid were also registered, indicating changes in bacterial metabolism. A pressure stress of 0·5 MPa during 300 h resulted in complete inactivation of O. oeni, but malolactic fermentation was still observed at some extent, showing that malolactic enzyme was not completely inactivated at these conditions. It was concluded that high pressure causes modification of O. oeni metabolism, and possibly in enzyme activities. SIGNIFICANCE AND IMPACT OF THE STUDY: This study demonstrates that high pressure affects the viability and metabolism of Oenococcus oeni on a culture medium, depending on the pressure intensity and holding time applied. These effects were particularly noteworthy on malolactic fermentation. After high pressure (HP)-stress of 100 MPa for 8 h, modifications in the activity of malolactic enzyme were detected, possibly due to a change in specificity. After a HP-stress of 300 MPa for 0·5 h, malolactic enzyme showed some residual activity, although O. oeni was completely inactivated. This study provides relevant information about the impact of high pressure on malolactic fermentation, opening interesting possibilities to the improvement of biocatalytic processes.

Mammary stimulation and maternal aggression in rodents: thelectomy fails to reduce pre- or postpartum aggression in rats.

In mice, tactile stimulation of the nipples appears to be critical for the onset of postpartum maternal aggression. Surgical removal of the nipples (thelectomy) blocks aggression if performed prior to parturition. In rats, indirect evidence suggests a similar role for nipple stimulation in maternal aggression. Two experiments were undertaken to determine whether thelectomy prior to mating reduces pregnancy-induced and/or postpartum aggression in this species. In the first, thelectomized and sham-thelectomized females were subjected to home cage tests (pups, if any, present) with unfamiliar male intruders on Gestation Days 18 and 21 and Lactation Days 3 and 5. Additional groups of thelectomized females were tested one time only on either Lactation Day 5 or 12. Thelectomized and control females were equally aggressive; postpartum, nearly all females in both groups attacked. Experiment 2 used females that were hysterectomized-ovariectomized (HO) on Gestation Day 16. Such females are not aggressive prior to initiating maternal behavior, but become highly aggressive (over 80% attacking) after commencing maternal care. Females again were thelectomized or sham-thelectomized prior to mating. On Day 16 HO was performed, and 48 hr later continuous exposure to pups was begun. After the females had displayed maternal behavior for 1.5-2 days, intruder tests were conducted. All females attacked at least once, with no differences between treatment groups. Thus thelectomy does not reduce maternal aggression in the rat. This finding, however, does not preclude a role for tactile ventral stimulation in mediating maternal aggression.