This review examines the role that oxidative stress, and protein oxidation in particular, plays in nutrition, metabolism and health of farm animals. The route by which redox homeostasis is involved in some important physiological functions and the implications of the impairment of oxidative status on animal health and diseases is also examined. Proteins have various and, at the same time, unique biological functions and their oxidation can result in structural changes and various functional modifications. Protein oxidation seems to be involved in pathological conditions such as respiratory diseases and parasitic infection; however some studies also suggest that protein oxidation plays a crucial role in the regulation of important physiological functions such as reproduction, nutrition, metabolism, lactation, gut health and neonatal physiology. As the characterization of the mechanisms by which oxidative stress may influence metabolism and health is attracting considerable scientific interest, the aim of this review is to present veterinary scientists and clinicians with various aspects of oxidative damage to proteins.

The decline in milk yield after peak lactation in dairy animals has long been a biological conundrum for the mammary biologist, as well as a cause of considerable lost income for the dairy farmer. Recent advances in understanding the control of the mammary cell population now offer new insights on the former, and a potential means of alleviating the latter. The weight of evidence now indicates that a change in mammary cell number, the result of an imbalance between cell proliferation and cell removal, is a principal cause of declining production. Further, it suggests that the persistency of lactation, the rate of decline in milk yield with stage of lactation, is strongly influenced by the rate of cell death by apoptosis in the lactating gland. Mammary apoptosis was first demonstrated during tissue involution after lactation, but has now been detected during lactation, in mammary tissue of lactating mice, goats and cattle. Those factors that determine the rate of cell death by apoptosis are as yet poorly characterized, but include the frequency of milking in lactating goats. Initial evidence suggests that nutrition also is likely to influence cell survival after peak lactation, an important factor being the degree of oxidative stress imposed by feed and the tissue's ability to deal with, and prevent damage by, reactive oxygen species. Comparison of cows in calf or not pregnant during declining lactation also indicates a likely influence of reproductive hormones, with oestradiol and progesterone acting to preserve mammary ductal and alveolar integrity during the dry period, while allowing a degree of apoptosis and cell replacement. In each case, the molecular mechanisms controlling mammary cell survival (or otherwise) are as yet poorly defined. On the other hand, more persistent lactations are likely to benefit animal welfare through fewer calvings and by placing less emphasis on maximal production at peak lactation, and modelling of persistent lactation with longer calving intervals indicates their likely economic benefits. In these circumstances, there is considerable incentive to elucidate the determinants of mammary apoptosis, and the factors controlling the dynamic balance between cell proliferation and cell death in the lactating mammary gland.

In the veterinary sector, many papers deal with the relationships between inflammation and oxidative stress. However, few studies investigate the mechanisms of action of oxidised molecules in the regulation of immune cells. Thus, authors often assume that these events, sometime leading to oxidative stress, are conserved among species. The aim of this review is to draw the state-of-the-art of the current knowledge about the role of oxidised molecules and dietary antioxidant compounds in the regulation of the immune cell functions and suggest some perspectives for future investigations in animals of veterinary interest.

Clay minerals are naturally occurring rock and soil materials primarily composed of fine-grained aluminosilicate minerals, characterized by high hygroscopicity. In animal production, clays are often mixed with feed and, due to their high binding capacity towards organic molecules, used to limit animal absorption of feed contaminants, such as mycotoxins and other toxicants. Binding capacity of clays is not specific and these minerals can form complexes with different compounds, such as nutrients and pharmaceuticals, thus possibly affecting the intestinal absorption of important substances. Indeed, clays cannot be considered a completely inert feed additive, as they can interfere with gastro-intestinal (GI) metabolism, with possible consequences on animal physiology. Moreover, clays may contain impurities, constituted of inorganic micronutrients and/or toxic trace elements, and their ingestion can affect animal health. Furthermore, clays may also have effects on the GI mucosa, possibly modifying nutrient digestibility and animal microbiome. Finally, clays may directly interact with GI cells and, depending on their mineral grain size, shape, superficial charge and hydrophilicity, can elicit an inflammatory response. As in the near future due to climate change the presence of mycotoxins in feedstuffs will probably become a major problem, the use of clays in feedstuff, given their physico-chemical properties, low cost, apparent low toxicity and eco-compatibility, is expected to increase. The present review focuses on the characteristics and properties of clays as feed additives, evidencing pros and cons. Aims of future studies are suggested, evidencing that, in particular, possible interferences of these minerals with animal microbiome, nutrient absorption and drug delivery should be assessed. Finally, the fate of clay particles during their transit within the GI system and their long-term administration/accumulation should be clarified.