Masters Theses

Date of Award

12-1995

Degree Type

Thesis

Degree Name

Master of Science

Major

Animal Science

Major Professor

James K. Miller

Committee Members

J.C. Walker, F.M. Hopkins

Abstract

The health of a dairy cow is of extreme economic importance to the dairy farmer especially at the time of parturition. Parturition and the period immediately before and after parturition are the most stressful times in the life of adult dairy cows. Most health problems will occur early in the cow's lactation cycle. It is an advantage to the farmer to have his or her cows in top physical condition as this time approaches. According to Shanks et al. (1981) mammary and reproductive costs were over 50% of the total health costs in the first 30 days of lactation. Because these are the two most important areas of production, they effect the income of the farmer the most. Reproductive and mammary gland diseases effect the quality and quantity of milk as well as the cost of the treatments (Shanks et al., 1981, and Vestwebber et al., 1984).

The health of the mammary gland is of extreme importance to the dairy farmer, because this is where the majority of his or her income is obtained. An animal with udder edema requires more labor to milk, is more prone to injury, and is under an extreme amount of stress (Dentine et al., 1983). Although the exact cause of udder edema is not known, there have been numerous proposal as to its origin (Vestwebber et al., 1984). Miller et al. (1993) reported a reduction in the number of animals with udder edema when an adequate amount of vitamin E and Se were received from the diet before parturition. This might suggest that oxidative stress could play a role in the incidence and severity of udder edema.

Oxidative stress is caused by a build up of oxygen free radicals in the cow's blood system. The reactive oxygen metabolites, which include superoxide and hydrogen peroxide, are produced as a result of normal metabolic functions. They are often involved in important physiological roles such as phagocytic action and enzymatic control (Rice-Evans et al., 1993). When produced at normal metabolic rates these free radicals are not harmful, however, if they are converted to more reactive species by transition metals, such as Fe and Cu, they can cause great harm to the body (Miller et al., 1993; Halliwell, 1991; Beger et al., 1990; and Groot, 1994).

Iron is essential for life so the body protects itself by sequestering Fe in the proteins, transferrin and ferritin. However in cases where Fe is excessive in the diet or during infection, inflammation and environmental stress, Fe may become available. This occurs because Fe binding sites become saturated allowing Fe to become decompartmentalized or nonspecifically bound. Decompartmentalized Fe then becomes the initiator of free radical chain-reactions. Iron can be involved in several different types of oxidative reactions. Iron catalyses the reaction between superoxide and hydrogen peroxide to produce the hydroxyl radical (Groot, 1994). The hydroxyl radical which is the most reactive radical (Burton, 1994), causes specific damage to phospholipids, proteins, carbohydrates, and DNA strands (Miller et al., 1993). Iron may also be involved in lipid peroxidation to form alkoxyl and peroxyl radicals (Halliwell, 1991).

It is important to terminate the free radical reactions before it causes extensive damage to the body. Antioxidants can prevent free radical reactions by several different mechanisms. There are at least three lines of defense against free radical damage (Miller and Madsen, 1994). First macromolecules compartmentalize transition elements preventing their catalytic activity. Second, antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase remove superoxide and peroxides before they can approach catalytic transition metals. Finally, chemical antioxidants terminate peroxidative chains initiated by free-radicals which escaped the first two lines of defense. These exogenous antioxidants include vitamin E which protects against lipid peroxidation (Bendich, 1993).

Unfortunately, it takes more than vitamin E to contain all free radical reactions. Vitamin E is ineffective against site specific radical damage. Site specific damage occurs when Fe is loosely bound to a protein and causes the formation of the hydroxyl radical at that site (Har-el and Chevion, 1991). Zinc, which only recently has been recognized as an antioxidant, can prevent site specific damage. Zinc prevents these reactions because of its similar chemical make up to Fe (Bettger et al., 1990). Zinc has the unique ability to displace Fe during redox reactions producing a non-reactive product (Har-el, 1991). Because so often dairy cattle diets contain high concentrations of Fe, it may be necessary to consider supplementation with Zn as a preventative measure for the damaging effect that decompartmentalized Fe may cause.

Parturition is an extremely stressful time for the animal, therefore it is possible that oxidative stress may increase the severity and the incidence of udder edema in dairy cows. Oxidative stress may cause udder edema by increasing membrane permeability or decreasing the production of reproductive hormones causing and increase in water retention (Vestwebber et al., 1984; Miller et al., 1993). This experiment was designed to test the effectiveness of vitamin E or Zn in reducing udder edema of heifers fed excess Fe.

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