This chapter examines the role that oxidative stress plays in ruminant medicine. We examine how redox homeostasis in involved in some physiological functions and we discuss the implications of the impairment of oxidative status on ruminant health and production. The study of oxidative stress is a relatively young field of research in ruminant medicine. The understanding of the role of oxidants and antioxidants in physiological and pathological conditions is rapidly increasing. Oxidative stress is an active field of research in ruminant medicine and has been implicated in numerous disease processes including sepsis, mastitis, acidosis, ketosis, enteritis, pneumonia, respiratory, and joint diseases. Compared to human medicine, only a limited number of conditions have been investigated in regard to the effects of oxidative stress in ruminants. Studies in cattle have been sporadic and mainly concerned with mastitis, pneumonia, and retained placenta. More recently, studies have been focused on metabolic diseases that affect dairy cows during the peripartum period. Numerous and rapidly evolving methodologies for evaluating oxidative stress are available to researchers and clinicians, each with their own distinct advantages and disadvantages. Differences in models and methodologies make it difficult to make meaningful comparisons, even for studies that seem quite similar superficially. With this in mind, it is the goal of this chapter to summarise the present knowledge of oxidative stress in ruminant medicine and to examine the basis of and evidence for the role of oxidative stress in ruminant health and production, highlighting the need for continued research on oxidative stress in ruminant medicine. Clarity of understanding of the pathophysiology of oxidative stress in ruminants will allow the design of specific antioxidant therapies. Future research should focus on the establishment of a reference panel of biomarker of oxidative stress to be used in ruminant medicine. The development of an oxidative stress index as an approach in ruminant and veterinary medicine is also discussed.

Oxidative Stress in Ruminants

Potential toxicity and feed value of onions for sheep

Dimethyl disulphide (DMDS), the main cause of brassica anaemia in ruminant animals, was determined in the blood of steers ingesting S-methylcysteine sulphoxide (SMCO) present in leafy brassicas. Blood samples were treated with Zn and dilute phosphoric acid and the DMDS reduced to methanethiol which was determined by gas chromatography headspace analysis. DMDS levels increased as the intake of SMCO with the brassicas progressed. They were maximal at the haemolytic crisis; thereafter, with the appearance of young red cells or reticulocytes, they declined sharply, but again increased as the new cells matured. The distribution of DMDS was; red cell 85%, plasma 15%. The distribution reached equilibrium in vitro in about 2 h.

Dimethyl disulphide in the blood of cattle fed on brassicas

The formation of reactive free radical species in sheep erythrocytes challenged with dimethyldisulphide, a brassica-derived haemolysin, has been investigated by electron spin resonance spectroscopy using the spin trap alpha-(4-pyridyl 1-oxide)-N-tert-butylnitrone. Erythrocytes exposed to this agent undergo a burst of free radical activity as demonstrated by the appearance of a spin adduct. The results suggest that haemolytic anaemia which can occur in sheep grazing forage brassicas is a consequence of oxidative stress.

The role of free radicals in brassica-induced anaemia of sheep: an ESR spin trapping study.

Kale of normal and low S-methyl-L-cysteine sulphoxide (SMCO) content was produced by growing the same cultivar in soils of normal (20–30 mg/kg) and low (5–10 mg/ kg) soil sulphate-S concentration. Compared with normal S plots, kale grown in low S plots showed little or no reduction in D.M. yield or total N content, but contained lower concentrations of inorganic sulphate, SMCO and glucosinolates.Replicated plots of normal and low SMCO kale were grazed by lambs for 12-week periods in two consecutive years, using a fixed crop allowance of 2·5 kg D.M./animal/ day. All animals were given injections of copper and iodine, and oral supplements of selenium, to ensure that effects upon animal performance could largely be attributed to differences in kale SMCO concentration.SMCO concentration in the diet consumed by lambs grazing normal and low SMCO kale was respectively 0·60 and 0·35% D.M. Following the onset of kale feeding, all animals developed subclinical haemolytic anaemia which stabilized by week 6, and was more marked during weeks 1–6 than during weeks 7–12. Animals grazing low SMCO kale showed a less severe anaemia than those grazing normal SMCO kale, which was associated with lower blood concentrations of dimethyl disulphide and Heinz bodies, and higher reduced glutathione (GSH) and packed cell volume (PCV) levels. Liveweight gain and wool growth were greater for lambs grazing low than normal SMCO kale during weeks 1–6, corresponding to the period of most severe haemolytic anaemia, but during weeks 7–12 there were no differences between the two groups.It was concluded that SMCO content depressed kale feeding value, with most of the depression occurring in the first 6 weeks of grazing, and that in these experiments the lambs were able to adapt to kale containing 0·6% D.M. as SMCO after 6 weeks of feeding. Endocrine factors involved in this adaptation are discussed.

The relative feeding value of kale ( Brassica oleracea ) containing normal and low concentrations of S-methyl-L-cysteine sulphoxide (SMCO)

Changes in bovine red cell plasma membrane properties were followed during onset and recovery phases of the Heinz body anaemia which accompanies intensive forage brassica feeding, and consequent S-methylcysteine sulphoxide ingestion and dimethyl disulphide generation. The onset of the haemolytic crisis shown by increased Heinz body counts and red cell osmotic fragility and by decreased haemoglobin levels, is accompanied by marked falls in blood glutathione (GSH) and cholesterol levels. Plasma membrane changes coinciding with these events include an increase in peroxidation levels and decreases in sulphydryl and cholesterol contents. The fall in relative microviscosity, indicated by fluorescence polarization measurements, suggests a decrease in lipid packing density in membranes with elevated peroxidation levels. Mechanisms underlying these changes are discussed, with special reference to disulphide exchange reactions of DMDS with GSH and other thiols.

Red Cell Membrane Changes in a Heinz Body Anaemia (Kale Anaemia)

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Red Cell Membrane Changes in a Heinz Body Anaemia (Kale Anaemia)