Olive oil consumption during pregnancy and lactation in rats influences mammary cancer development in female offspring.
This study examined the effects of variety and quantity of dietary fat consumed by rats during pregnancy and lactation on female offspring's response to chemically induced mammary cancer. Groups of six female rats were fed diets containing 7% corn oil (7-CO), 15% CO (15-CO), 7% olive oil (7-OO), or 15% OO (15-OO) for 5 wk prior to, and during, pregnancy and lactation. Female offspring (n = 15 per group) were fed a 7-CO diet, and mammary cancer was induced with 7,12-dimethylbenz[a]anthracene (DMBA). Three months following cancer induction tumor incidence and size were recorded, and markers of apoptosis, serum estrogen concentrations, and hepatic phase II enzymes were measured. Tumor incidence was 47% in offspring born to mothers fed the 7-OO diet, rose to 67% in 7-CO and 15-OO offspring, and reached 86% in 15-CO. A trend toward smaller tumors was observed in the 7-OO group, and offspring of mothers fed high-fat diets had significantly more tumors. Estradiol levels at the end of lactation were significantly lower in mothers fed 7-OO but were similar in all groups of offspring. In tumor tissue, Bcl-2 expression was highest in the 15-CO offspring, and Bak expression was significantly higher in rats exposed to OO. A distinct trend toward increased caspase-3 expression (20 kDa) was observed in the 7-OO offspring, and both low-fat diets significantly elevated caspase activity. In healthy mammary tissue, rats exposed to low-fat diets had significantly higher caspase-3 (32-kDa) levels, and caspase-3 activity was significantly higher in the healthy tissue from both OO groups. Hepatic quinone reductase activity was significantly lower in offspring of mothers fed the low-fat diets. These results indicate that perinatal exposure to OO may have a protective effect against future development of mammary cancer in female offspring, whereas high-fat diets fed to pregnant and lactating rats, in particular CO, may be deleterious.
Stark
Aliza H
AH
The Hebrew University of Jerusalem, Faculty of Agricultural, Food and Environmental Quality Sciences, Rehovot, Israel.
Kossoy
George
G
Zusman
Itshak
I
Yarden
Ganit
G
Madar
Zecharia
Z
D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D053148:Caspase 3; D020169:Caspases / Q000187:drug effects; D004958:Estradiol / Q000097:blood; D005260:Female; D005982:Glutathione Transferase / Q000187:drug effects; D007774:Lactation / Q000502:physiology*; D008099:Liver / Q000201:enzymology; D015674:Mammary Neoplasms, Animal / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D008431:Maternal-Fetal Exchange / Q000502:physiology*; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000187:drug effects; D000069463:Olive Oil; D010938:Plant Oils / Q000008:administration & dosage / Q000494:pharmacology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley
D000069463:Olive Oil; D010938:Plant Oils; D004958:Estradiol; D016660:NAD(P)H Dehydrogenase (Quinone); D005982:Glutathione Transferase; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases