Journal of Dairy Research

Research Article

Production of hydrogen peroxide by a small molecular mass compound in milk from Holstein cows with high and low milk somatic cell count

Senkiti Sakaia1 c1, Eriko Nonobea1, Takahiro Satowa2, Kazuhiko Imakawaa1 and Kentaro Nagaokaa1

a1 Department of Animal Breeding, The Graduate School of Agricultural and Life Sciences, The University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo 113-8657, Japan

a2 Department of Cell Biology, The Graduate School of Bioresource Sciences, Nihon University, Kameino 1866, Fujisawa 252-8510, Japan

Abstract

Mastitis is the most frequent and prevalent production disease in dairy herds in developed countries. Based on a milk somatic cell count (SCC) of either >300 000 or <200 000 cells/ml in this study, we defined the quarter as either inflamed or uninflamed, respectively. The electrical conductivity (EC) of milk was used as an indicator of udder epithelial cell damage. We determined the amount of H2O2 produced by utilizing a small molecular weight compound in milk, and examined the characteristics of H2O2 production and EC in milk from inflamed and uninflamed quarters. In cows with milk of delivery grade (control population), H2O2 production and EC were 3·6±1·3 nmol/ml and 5·4±0·4 mS/cm (mean±sd), respectively. In 37 inflamed quarter milk samples, the production of H2O2 was 1·9±1·0 nmol/ml and was significantly smaller than that in the control population (P<0·01). Production of H2O2 was moderately but significantly correlated with EC (r<−0·71). In 20 cows with inflamed quarters, the production of H2O2 in milk from inflamed quarters was significantly smaller than that in milk from uninflamed quarters (P<0·01). In 18 out of 20 cows, milk from inflamed quarters showed the smallest H2O2 production among all tested quarters in each cow. We conclude that inflammation caused a decrease in H2O2 production in milk. In this study, we present parameters for evaluating the lactoperoxidase/H2O2/thiocyanate antibacterial defence system in bovine milk.

(Received December 28 2007)

(Accepted March 27 2008)

Correspondence:

c1 For correspondence; e-mail: asenkiti@mail.ecc.u-tokyo.ac.jp