Localized mammary gland changes in milk composition and venous blood metabolite concentrations result from sterile subclinical mastitis.

Subclinical mastitis reduces milk yield and elicits undesirable changes in milk composition, but the mechanisms resulting in reduced milk production in affected mammary glands are incompletely understood. This study investigated the effects of sterile inflammation on mammary gland metabolism by assessing changes in milk and venous blood composition. Mid-lactation primiparous Holstein cows (n = 4) had udder halves randomly allocated to treatments; quarters of 1 udder half were infused with 2 billion cfu of formalin-fixed Staphylococcus aureus (FX-STAPH) and quarters of the opposite udder half were infused with saline (SAL). Blood samples were collected from the right and left subcutaneous abdominal veins in 2.6 h intervals until 40 h postchallenge and analyzed for blood gas and metabolite concentrations. Milk from FX-STAPH udder halves had significantly increased SCS by the first milking at 8 h postchallenge. By 16 h postchallenge, FX-STAPH udder halves had increased concentrations of protein and lactate and lower lactose concentrations than SAL udder halves. Milk fat concentrations, milk yields, ECM yields, and the ferric reducing antioxidant power of milk were not significantly different between SAL and FX-STAPH udder halves. Venous blood of FX-STAPH halves had marginally greater concentrations of saturated O2, partial pressures of O2, and glucose concentrations than SAL halves. Conversely, total and partial pressures of CO2 did not differ between udder half treatments, suggesting a shift in local metabolite utilization in FX-STAPH udder halves. These results indicate that changes in milk composition resulting from mastitis are accompanied by changes in some key blood metabolite concentrations. The shift in venous blood metabolite concentrations, along with the marked increase in milk lactate, suggests that local mammary tissue or recruited immune cells, or both, alter metabolite usage in mammary tissues. Future studies are needed to quantify the uptake of key milk precursors during mastitis.

Effects of oyster glycogen intramammary challenge on primiparous cow milk somatic cell counts, milk yields, and milk composition.

Mastitis is a common and costly disease in the dairy industry that reduces milk production in affected mammary glands. The local mechanisms that result in reduced milk production of affected mammary glands are incompletely understood; elucidation of these mechanisms is dependent on the use of hypothesis testing studies, but few experimental models exist. The objective of this study was to develop a mastitis challenge model, using a split udder design, to reduce milk yields by approximately 15% in udder halves challenged with oyster glycogen, a known inducer of leukocyte recruitment, relative to udder halves treated with saline. Four primiparous Holstein cows in mid lactation were used. One udder half of each cow was randomly selected and challenged with oyster glycogen (OYGLN), and the opposite udder half was treated with saline (SAL). Milk yields and components were measured at each milking (3×/d) for 3 d postchallenge. No signs of clinical mastitis were observed. Milk somatic cell scores, yields, and components were similar between OYGLN and SAL udder halves at time of challenge. Milk somatic cell scores markedly increased in OYGLN halves postchallenge and were greater than SAL halves for the duration of the trial. Lactose concentrations of OYGLN udder halves were transiently lower than in SAL udder halves, but protein concentrations were greater at 2 milkings postchallenge in OYGLN halves. Milk yields and energy-corrected milk yields did not differ between OYGLN and SAL udder halves overall, nor at any postchallenge milking. A single intramammary challenge of oyster glycogen was unsuccessful in eliciting a disparity in milk yields between challenged and saline control udder halves despite the marked leukocyte infiltration observed in the former. These results indicate an incomplete understanding of how milk yields are reduced in mammary glands affected by subclinical mastitis and that transient somatic cell recruitment and infiltration alone do not directly reduce milk yields during subclinical mastitis.

Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain.

Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting. This study investigated the effect of well-established swimming training protocol on lipid peroxidation and components of antioxidant system in the rat brain. Male Wistar rats were randomized into trained (5 days/week, 8 weeks, 30 min; n=8) and non-trained (n=7) groups. Forty-eight hours after the last session of exercise, animals were euthanized and the brain was collected for oxidative stress analysis. Swimming training decreased thiobarbituric acid reactive substances (TBARS) levels (P<0.05) and increased the activity of the antioxidant enzyme superoxide dismutase (SOD) (P<0.05) with no effect on brain non-enzymatic total antioxidant capacity, estimated by FRAP (ferric-reducing antioxidant power) assay (P>0.05). Moreover, the swimming training promoted metabolic adaptations, such as increased maximal workload capacity (P<0.05) and maintenance of body weight. In this context, the reduced TBARS content and increased SOD antioxidant activity induced by 8 weeks of swimming training are key factors in promoting brain resistance. In conclusion, swimming training attenuated oxidative damage and increased enzymatic antioxidant but not non-enzymatic status in the rat brain.

Swimming training attenuates oxidative damage and increases enzymatic but not non-enzymatic antioxidant defenses in the rat brain

Although it is well known that physical training ameliorates brain oxidative function after injuries by enhancing the levels of neurotrophic factors and oxidative status, there is little evidence addressing the influence of exercise training itself on brain oxidative damage and data is conflicting. This study investigated the effect of well-established swimming training protocol on lipid peroxidation and components of antioxidant system in the rat brain. Male Wistar rats were randomized into trained (5 days/week, 8 weeks, 30 min; n=8) and non-trained (n=7) groups. Forty-eight hours after the last session of exercise, animals were euthanized and the brain was collected for oxidative stress analysis. Swimming training decreased thiobarbituric acid reactive substances (TBARS) levels (P<0.05) and increased the activity of the antioxidant enzyme superoxide dismutase (SOD) (P<0.05) with no effect on brain non-enzymatic total antioxidant capacity, estimated by FRAP (ferric-reducing antioxidant power) assay (P>0.05). Moreover, the swimming training promoted metabolic adaptations, such as increased maximal workload capacity (P<0.05) and maintenance of body weight. In this context, the reduced TBARS content and increased SOD antioxidant activity induced by 8 weeks of swimming training are key factors in promoting brain resistance. In conclusion, swimming training attenuated oxidative damage and increased enzymatic antioxidant but not non-enzymatic status in the rat brain.