Effect of abomasal or ruminal administration of citrus pulp and soybean oil on milk fatty acid profile and antioxidant properties.

Soybean oil (SBO) is rich in polyunsaturated fatty acids (FA) and rumen bypass of SBO can contribute to increase the polyunsaturated FA proportion in milk fat. Citrus pulp (CPP) is a source of antioxidants but there is little information on the effects of CP administration on milk properties. This study was performed to determine the role of rumen microorganisms in the transfer of antioxidants from CPP into milk when cows receive SBO as a source of polyunsaturated FA. Four ruminally fistulated lactating Holstein cows were assigned to a 4 × 4 Latin square design with a 2 × 2 factorial arrangement of treatments: (1) SBO administered in the rumen; (2) SBO infused in the abomasum; (3) SBO + CPP administered in the rumen; and (4) SBO + CPP infused in the abomasum. Product and site of administration had no effect on yield of milk components. Concentrations of total polyphenols and flavonoids, reducing power and production of conjugated diene (CD) hydroperoxides in milk were not affected by products, but infusion in the abomasum compared with administration in the rumen increased production of CD. Milk fat FA profile was not affected by products. However, cows infused in the abomasum compared with those administered in the rumen showed lower proportions of short-chain and monounsaturated FA and higher proportions of polyunsaturated, omega 3 and omega 6 FA in milk fat, which resulted in enhanced health-promoting index of milk. Administration of SBO and CPP (0.2 + 1.0 kg/d) in the rumen or the abomasum resulted in similar milk antioxidant properties, thus suggesting that the rumen microbes have little involvement in the metabolism of antioxidants from CPP.

α-Tocopherol administration blocks adaptive changes in cell NADH/NAD+ redox state and mitochondrial function leading to inhibition of gastric mucosa cell proliferation in rats.

In experimentally induced chronic gastritis, a compensatory mucosal cell proliferation occurs with enhanced glucose oxidative metabolism linked to lipoperoxidative events. Therefore, this study was aimed at assessing the participation of cell NAD/NADH redox state and mitochondrial functions during gastric mucosa proliferation and the effects of in vivo α-tocopherol (vitamin E) administration. Glucose oxidation and oxygen consumption were tested in gastric mucosa samples obtained from rats with gastritis and from those also treated with α-tocopherol. Gastric mucosal mitochondria were isolated and structural and functional parameters were determined. Succinate oxidation, ADP phosphorylation, mitochondrial enzyme activities, and membrane lipid composition were measured. In addition, parameters indicative of cellular NAD/NADH redox state, proliferation, apoptosis, and nitric oxide (NO) metabolism were also determined. After ethanol withdrawal, the damaged gastric mucosa increased glucose and oxygen consumption, events associated with a more reduced cytoplasmic NAD/NADH ratio. Enhanced mitochondrial oxidative phosphorylation and increased mitochondrial enzyme activities occurred early, accompanied by recovery of lost mitochondrial protein and lipid composition in the gastric mucosa, events associated with increased NO production. When mitochondrial function and structural events were normalized, apoptosis was initiated as assessed by the mitochondrial Bax/Bcl2 ratio. Treatment with α-tocopherol inhibited cell proliferation and blocked enhanced glucose utilization, mitochondrial substrate oxidation, and changes in redox state, delaying the onset of these adaptive metabolic changes, whereas it inhibited cell proliferation. In conclusion, α-tocopherol could abolish damage-induced "stress" signaling by desynchronizing mitochondrial adaptive responses, including mitochondria biogenesis, and consequently NAD/NADH redox, which seems to regulate gastric mucosal cell proliferation.