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Title: MODULATION OF GROWTH PERFORMANCE IN DISEASE: REACTIVE NITROGEN COMPOUNDS AND THEIR IMPACT ON CELL PROTEINS

Author
item Elsasser, Theodore
item Kahl, Stanislaw
item RUMSEY, THERON - USDA, ARS, RETIRED
item BLUM, J. - UNIV OF BERNE SWITZERLAND

Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/6/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: All animals experience varying degrees of stresses in their lives. Most of the time the body's response to stress is such that the body readjusts naturally and restores health. In some severe reactions to stresses, infection stress in particular, processes in the body that otherwise restore health become over reactive to the stress and participate in the extended duration of poor health. A part of the reason that this occurs i that some nitrogen compounds are formed in excess. These excess nitrogen compounds like nitric oxide breakdown into other compounds that are very chemically reactive and cause normal cell proteins to be modified by the incorporation of some nitrate molecules onto important amino acids in the proteins. When this occurs, the biological function of the protein is changes and often lost. Thus is this process happens to cell proteins that regulate growth, the animal can not regulate its growth and growth is stunted. Controlling the overproduction of these chemically reactive nitrogen compounds may provide a means of maintaining good health and growth in animals.

Technical Abstract: During life, all animals encounter situations that challenge their capability for optimal growth. In reacting to immune challenges in the form of disease, homeostatic mechanisms attempt to overcome disharmony of the body's internal environment. The overall impact of stress revolves around a dynamic relationship between the level of challenge imparted on physiological systems and the degree of host response that is mounted in detecting and reacting to the stress. In growing animals, the majority of milder stress encounters are manifest in terms of energetic efficiencies and periods of reduced anabolism. In contrast, severe stress is often characterized by frank catabolism and tissue wasting. In some instances a level of stress (that might be termed a "stress breakpoint") is reached at which time the host response itself contributes to the cascade of negative effectors that cause further illness. These "breakpoint" responses are characterized by more intense acute responses to stress or a much more protracted duration of the response. Key to understanding how growth in the young animal responds to infectious stresses is the recognition that (a) when immune responses that normally maintain health go awry, the reporters of the immune system (cytokines and nitric oxide cascade) can contribute to stress-disease processes and (b) reactive nitrogen compounds derived from nitric oxide and superoxide anion can modify intracellular proteins and block otherwise normal biochemical processes that regulate cell function.