Pharmacokinetics of oxytetracycline in broiler chickens following different routes of administration.

The aim of this study was to determine the pharmacokinetics of oxytetracycline (OTC) in broiler chickens following intravenous (IV), intramuscular (IM), subcutaneous (SC) and oral (PO) administrations at a dose of 15 mg/kg bodyweight. Plasma concentrations of OTC were determined using liquid chromatography-tandem mass spectrometry and non-compartmental pharmacokinetic analysis was then conducted. The absorption half-life time was 1.23 ± 0.36 h, 1.19 ± 0.52 h, and 0.49 ± 0.38 h after IM, SC and PO administration, respectively. The elimination half-life time was 27.41 ± 6.06 h, 10.23 ± 4.20 h, 7.83 ± 0.56 h, and 14.86 ± 9.23 h, and the mean residence time was 9.67 ± 1.7 h, 11.45 ± 1.76 h, 11.38 ± 0.59 h, and 10.37 ± 3.91 h after IV, IM, SC and PO administration, respectively. Bioavailability was 76.88 ± 12.90%, 92.20 ± 10.53% and 12.13 ± 4.56% after IM, SC and PO administration, respectively, which indicated that OTC is poorly absorbed from the gastrointestinal tract in broiler chickens.

Effect of enrofloxacin and chlorpyrifos on the levels of vitamins A and E in Wistar rats.

This study investigates the effects of enrofloxacin and chlorpyrifos, and their combination on vitamin A and E concentrations in the liver of rats. Results of this study indicated a reduction in the contents of vitamins A and E in the liver, which persisted for the entire period of the experiment. Vitamins A and E concentrations were slightly decreased (2-7%) in enrofloxacin-treated rats. In the group of rats intoxicated with chlorpyrifos, a significant decrease in the level of vitamin A was observed up to the 24th hour, and for vitamin E up to the 3rd day from the discontinuation of intoxication with the compounds under study. In the enrofloxacin-chlorpyrifos co-exposure group reduced vitamins A and E level was also noted. The greatest fall in vitamin A level was observed after 3h, while the contents of vitamin E decreased progressively up to the 3rd day. Changes in this group were less pronounced in comparison to the animals intoxicated with chlorpyrifos only.

Beavers indicate metal pollution away from industrial centers in northeastern Poland.

Heavy metals are persistent environmental contaminants, and wild animals are increasingly exposed to the harmful effects of compounds of anthropogenic origin, even in areas distant from industrial centers. We used atomic absorption spectrometry to determine levels of cadmium (Cd), lead (Pb), copper (Cu), and zinc (Zn) in liver and kidney of wild Eurasian beavers (Castor fiber) in Poland. Cd concentrations in liver (0.21 ± 0.44 µg/g) and in kidney (2.81 ± 4.52 µg/g) were lower in juvenile than in adult beavers. Pb concentrations in liver (0.08 ± 0.03 µg/g) and kidney (0.08 ± 0.03 µg/g) were similar among all individuals, while both Cu and Zn levels were higher in liver (Cu 9.2 ± 4.5 µg/g; Zn 35.7 ± 3.5 µg/g) than in kidney (Cu 3.7 ± 1.1 µg/g; Zn 21.5 ± 2.7 µg/g). Cu levels also differed between juveniles and adults. We reviewed the literature reporting metal concentrations in beavers. Our results indicate metal contamination in beavers away from important industrial emission sources and suggest the natural environment should be regularly monitored to ensure their levels are below recommended, legal values.

Prostaglandin E2 down-regulates the expression of CD25 on bovine T cells, and this effect is mediated through the EP4 receptor.

A crucial event in the initiation of an immune response is the activation of T cells, which requires IL-2 binding to its high-affinity IL-2 receptor for optimal signaling. The IL-2 receptor α-chain (CD25) is needed for the high affinity binding of IL-2 to effector cells and is potently induced after T cell activation. The aim of this research has been to determine whether prostaglandin E2 (PGE2) affects the CD25 expression on bovine T cells, and if it does, then which of the PGE2 receptor (EP) subtype(s) mediate(s) this effect. Herein, we report that exposure of peripheral blood mononuclear cells (PBMC) to PGE2 considerably reduces the percentage and absolute counts of CD25(+)CD4(+), CD25(+)CD8(+) and CD25(+)WC1(+) T cells, significantly increases the value of these parameters with respect of CD25(-)CD4(+), CD25(-)CD8(+) and CD25(-)WC1(+) T cells, and does not affect counts of the total populations of CD4(+), CD8(+) and WC1(+) T cells. These results indicate that PGE2 down-regulates the CD25 expression on bovine T cells. Moreover, we show that the selective blockade of EP4 receptor, but not EP1 and EP3 receptors, prevents this effect. Interestingly, the exposure of PBMC to a selective EP2 receptor agonist leads to a substantial increase in the percentage and absolute number of CD25(+)CD4(+), CD25(+)CD8(+) and CD25(+)WC1(+) T cells. In conclusions, the PGE2-induced down-regulation of CD25 expression on bovine CD4(+), CD8(+) and WC1(+) T cells should be considered as immunosuppressive and anti-inflammatory action, because these lymphocytes primarily represent effector cells and adequate CD25 expression is essential for their correct functioning. The PGE2-mediated down-regulation of the CD25 expression on bovine T cells is mediated via the EP4 receptor, although selective activation of the EP2 receptor up-regulates the CD25 expression on these cells. Thus, with respect to the effect of PGE2 on the CD25 expression on bovine T cells, EP4 receptor serves as an inhibitory receptor, whereas EP2 receptor functions as a stimulatory receptor. The fact that non-selective stimulation of EP receptors, i.e. triggered by PGE2, leads to weaker CD25 expression proves that inhibitory actions prevail over stimulatory ones. These results indicate the possibility of pharmacological manipulation of the CD25 expression on T cells via selective antagonists and agonists of EP2 and EP4 receptors.