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KMID : 0900919970210040325
Korean journal of Animal Reproduction
1997 Volume.21 No. 4 p.325 ~ p.333
Artificial Induction of Environmental Mammary Stress by Temperature and Micro-organism Causing Mastitis and Modulation of Mammary Growth by Adenosine, IGF-I and Prolatin In Vitro



Lee Chang-Soo
Park Choon-Keun
Hong B. J.
Abstract
Recent evidence indicates that growth factors modulate response of mammary epithelial cells to environmental stress. The objective of this study was to examine the cellular and biochemical responses of mammary tissue to environmental stress caused by artificial mastitis. For experimental a, pp.oach, toxins of most mastitis causing organisms(Staph. aureus or Strep. agalactiae) and heat stress(42^{circ}C) were artificially exposed to mammary tissue. Effects of these environmental stresses on cell growth, cell death and heat shock protein synthesis were examined. Lactating mammary tissure were cultured under basal medium(DMEM) su, pp.emented with insulin(10mutextrm{g}/ml) and aldosterone(1mutextrm{g}/ml). All treatment groups in heat stress at 42^{circ}C incubation significantly decreased DNA synthesis rates in comparison with those at 39^{circ}C(P<0.05), however, these decreased DNAa synthesis rates were recovered by addition of adenosine(10muM) and IGFI(10ng/ml). Similar results were obtained when tissue growth rates were measured by DNA content/tissue. Strep. agalactiae toxin did not significantly decreased DNA content/tissue in comparison with no treatment of bacterial toxin with or without heat stress, however, tended to decrease DNA contents/tissue without heat stress. In the fluorography analysis, heat stress(42^{circ}C incubation) slightly increased 35S-methoionine labelled 70kd protein synthesis. These results indicate that environmental stress caused by artificial mastitis slightly decreased mammary growth or mammary size, however, these results could be recovered by addition of adenosine and IGF-I.
KEYWORD
environmental stress, mammary tissue, bacterial toxin, heat stress, mammary growth, adenosine, IGF-I, prolactin
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