NUTRITION DURING PREGNANCY, LACTATION, INFANCY, AND CHILDHOOD
Location: Children Nutrition Research Center (Houston, Tx)
Title: INCREASED MAMMARY GLAND OXIDATIVE DAMAGE AND APOPTOSIS DURING PROLONGED LACTATION IN THE MOUSE IS LITTLE AFFECTED BY OVEREXPRESSION OF DES(1-3)HIGF-I.
| Hadsell, D. - BAYLOR COLL MEDICINE |
| Torres, D. - BAYLOR COLL MEDICINE |
| George, J. - BAYLOR COLL MEDICINE |
Submitted to: Journal of Dairy Science
Publication Type: Abstract Only
Publication Acceptance Date: March 1, 2005
Publication Date: July 1, 2005
Citation: Hadsell, D., Torres, D., George, J. 2005. Increased mammary gland oxidative damage and apoptosis during prolonged lactation in the mouse is little affected by overexpression of des(1-3)hIGF-I [abstract]. Journal of Dairy Science. 88(Suppl. 1):77.
Interpretive Summary: Interpretive Summary not needed for this 115.
Prolonged lactation in the mouse is associated with decreased capacity to produce milk and loss of secretory tissue. This loss of function is delayed in transgenic mice that overexpress des(1-3)hIGF-I (WAP-DES). A primary goal of these studies was to determine the relationship between mammary cell apoptosis and oxidative damage during normal and prolonged lactation. A second goal was to determine if reduced mammary cell apoptosis occurs in WAPDES mice during prolonged lactation. The percentage of TUNEL-positive mammary cells present in the mammary gland during early and prolonged lactation was analyzed in two separate studies. In study 1, TUNEL staining and mammary protein carbonyl content (CC) was compared in mammary tissue samples collected from lactating mice on days 1, 2, 3, 5, 10, 35, and 57 post partum (4-10 animals/day). In study 2 TUNEL analysis was done on mammary tissue samples collected during peak lactation (day 8) or prolonged lactation (day 37) from either nontransgenic or WAP-DES dams (4 -12 dams per time-genotype combination). A third study compared both mammary CC and the content of 8-hydroxy 2'-deoxyguanosine (8-OG) in mitochondrial DNA isolated from glands collected at day 2, 10 and 35 postpartum (3-5 animals/day). In both TUNEL studies, percent apoptosis was lowest at peak lactation (study 1, day 10, 0.2±0.04%; study 2, day 8, 0.5±0.1%) and increased (P<0.05) 2- to 3-fold with prolonged lactation. Apoptosis in mammary tissue from the WAP-DES mice was similar (P>0.05) to that of nontransgenic mice. Both markers of oxidative damage change with day postpartum (p<0.05). Oxidative damage was high on day 2 decreased on day 10 and then increased on day 35 postpartum (CC, 3.1±0.2, 1.8±0.2, 2.4±0.2 nmole/mg protein respectively; 8-OG, 6.1±0.7, 4.4±0.8, 9.3±.7nmole/L mitochondrial extract, respectively). These results support the conclusion that apoptosis in association with cellular oxidative damage is increased in the mammary gland during prolonged lactation.