We previously reported changes in gene expression in mammary tissue from non-inflamed mammary glands adjacent to an inflamed gland challenged with lipopolysaccharide (LPS). We determined if changes in the expression of selected genes in non-inflamed glands would be replicated in RNA isolated from milk fat. Cows were milked twice daily prior to experiment. Per cow, one mammary gland (QLPS) was randomly assigned to receive an intramammary infusion of 50 µg LPS immediately after morning milking on d-0. The ipsilateral (QI) and contralateral (QC) mammary glands adjacent to QLPS remained untreated. Quarter foremilk samples from all mammary glands were collected on d-1 and d-0 for milk composition and isolation of RNA for quantification of selected genes via quantitative polymerase chain reaction. Symptoms of clinical mastitis developed only in QLPS and were apparent within 3 h post-challenge. In QI and QC, lactose percentages were lower at 12 h post-challenge compared to d-1, but milk fat and protein contents were not different. For gene expression, 7 of 13 selected genes were differentially regulated in non-inflamed glands. In QI but not QC, LALBA expression was lower at 12 h post-challenge than on d-1. One gene of interest, LPIN1, was significantly upregulated in QI and QC but downregulated in QLPS at 12 h post-challenge. Five additional immune or stress-related genes were significantly upregulated in QLPS and, to a lesser but significant degree, in QI and QC compared to d-1. Notably, expression of two immune genes (NFKBIA, PTX3) was significantly greater in QI than QC despite QI having a numerically lower somatic cell count. Minor changes in the composition of milk secreted by non-inflamed mammary glands were linked to several immune and stress responses in those glands. Further, individual non-inflamed mammary glands responded differently depending on their position relative to the mastitic gland.

α-Lipoic acid (ALA) has been termed the ‘ideal’ antioxidant, a readily absorbed and bioavailable compound capable of scavenging a number of free radicals, and it has been used for treating diseases in which oxidative stress plays a major role. The present study was designed to gain a better understanding for the positive effects of ALA on the models of acute and chronic inflammation in rats, and also determine its anti-oxidative potency. In an acute model, three doses of ALA (50, 100 and 200 mg/kg) and one dose of indomethacin (25 mg/kg) or diclofenac (25 mg/kg) were administered to rats by oral administration. The paw volumes of the animals were calculated plethysmometrically, and 0·1 ml of 1 % carrageenan (CAR) was injected into the hind paw of each animal 1 h after oral drug administration. The change in paw volume was detected as five replicates every 60 min by plethysmometry. In particular, we investigated the activities of catalase, superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR), inducible NO synthase (iNOS) and myeloperoxidase (MPx), and the amounts of lipid peroxidation (LPO) or total GSH in the paw tissues of CAR-injected rats. We showed that ALA exhibited anti-inflammatory effects on both acute and chronic inflammations, and a strongly anti-oxidative potency on linoleic acid oxidation. Moreover, the administration of CAR induced oedema in the paws. ALA significantly inhibited the ability of CAR to induce: (1) the degree of acute inflammation, (2) the rise in MPx activity, (3) the increases of GST and iNOS activities and the amount of LPO and (4) the decreases of GPx, GR and SOD activities and the amount of GSH. In conclusion, these results suggest that the anti-inflammatory properties of ALA, which has a strong anti-oxidative potency, could be related to its positive effects on the antioxidant system in a variety of tissues in rats.