[Isolation, identification, and degrading effect of a pyrene-degrading strain SE12].

Using pyrene as the sole carbon and energy source, and by the method of plate sublimation, a strain SE12 was isolated from a contaminated soil near Woniushan Coking Plant in Xuzhou, China. According to the morphological, biochemical, and 16S rDNA analyses, this strain was identified as Mycobacterium sp., with 98% of homology to the rapid-growth nonpathogenic strain M. austroafricanum ATCC 33464. The optimum pH and temperature for the degradation of pyrene by SE12 were pH 9 and 30 degrees C. When the soil samples were added with 100 and 200 mg x kg(-1) of pyrene and inoculated with 10(7) CFU x g(-1) of SE12, the degradation rates of pyrene reached to 97% and 99%, respectively after 28 days incubation at 30 degrees C. By using primer-pairs nidAF/nidAR and nidBF/nidBR for amplification of ring-hydroxylating dioxygenase genes, it was shown that SE12 had the fragments of encoded large and small subunits of dioxygenase genes. Sequence analysis showed that these fragments were highly homologous to the known dioxygenase genes from pyrene-degrading Mycobacteria sp.

Antidepressants modulate the in vitro inhibitory effects of propofol and ketamine on norepinephrine and serotonin transporter function.

Norepinephrine transporter (NET) and serotonin transporter (SERT) proteins regulate norepinephrine (NE) and serotonin via their reuptake function and are targets of antidepressants action. Several intravenous (IV) anesthetics have been shown to inhibit NET and SERT. The interactions between antidepressants and anesthetics on transporter function, however, are not well studied. We examined the effect of different IV anesthetics on NET and SERT function, with and without chronic antidepressant pretreatment, by measuring NE or 5-hydroxytryptamine (5-HT) uptake and determined NET and SERT protein expression via immunoblotting. Both ketamine and propofol inhibited NET dose-dependently (propofol 10(-4)M -22%+/-5.6%, and propofol 10(-3)M -35%+/-5.7%; ketamine 10(-4)M -23%+/-4.1% and ketamine 10(-3)M -73%+/-2.9%); and SERT (propofol 10(-4)M -11%+/-4.3% and propofol 10(-3)M -23%+/-3.8%; ketamine 10(-4)M -29%+/-5.2% and ketamine 10(-3)M -63%+/-6.4%). Etomidate and thiopental had no effect on either NET or SERT function. Desipramine and fluoxetine, specific inhibitors of NET and SERT, respectively, both enhanced the inhibitory effects of propofol but reduced the inhibitory effects of ketamine on NET and SERT functions. IV anesthetics treatment did not change transporter protein expression in the presence of its respective inhibitor. Our results demonstrate that both ketamine and propofol inhibited SERT and NET function, but the inhibition was differentially modulated by antidepressants. Therefore, in the clinical context, this would suggest that patients receiving antidepressant treatments might have altered response to IV anesthetics in an agent-specific manner.

Perinatal cocaine exposure reduces myocardial norepinephrine transporter function in the neonatal rat.

Norepinephrine transporter (NET) mediates the active removal of norepinephrine (NE) released from sympathetic nerve terminals via reuptake, and NET function and expression can be regulated by cocaine. NET expression and its regulation by cocaine in the developing sympathetic nervous system during early postnatal period, however, have not been examined. We quantified immunodetectable NET protein expression in the neonatal rat heart to examine the developmental pattern of myocardial NET during the first 2 weeks after birth. To assess sympathetic innervations, we simultaneously quantified the expression of myocardial tyrosine hydroxylase (TH). Timed pregnant rats received daily intragastric treatment with saline (CTL) or cocaine at 60 mg/kg (Coc) from Gestational Day 2 until parturition. After birth, nursing mothers continued to receive the same treatment. The expression of myocardial TH and NET in neonatal rats were then studied at 1 day (Postnatal Day 1, PD1), 7 days (PD7) or 14 days (PD14) of age. We observed a similar age-dependent increase in the expression for myocardial NET and TH during the first 2 weeks of postnatal life, in both CTL and Coc animals. While myocardial TH was significantly up-regulated following perinatal cocaine exposure, no significant change in immunodetectable myocardial NET protein was evident. To further examine whether NET function might be affected by perinatal cocaine exposure, we performed NE uptake in myocardial membranes from PD14 CTL and Coc rats. We found that NE uptake was reduced at PD14 in the cocaine-treated group. Our results indicate that myocardial NET and TH are both developmentally regulated. Furthermore, our results indicate that perinatal exposure to cocaine did not change NET protein expression but impaired myocardial NET function in the neonatal rat.