Ovariectomy attenuates dendritic growth in hormone-sensitive spinal motoneurons

The lumbar spinal cord of rats contains the sexually dimorphic, steroid-sensitive spinal nucleus of the bulbocavernosus (SNB). Dendritic development of SNB motoneurons in male rats is biphasic, initially showing exuberant growth through 4 weeks of age followed by a retraction to mature lengths by 7 weeks of age. The initial growth is steroid dependent, attenuated by castration or aromatase inhibition, and supported by hormone replacement. Dendritic retraction is also steroid sensitive and can be prevented by testosterone treatment, but is unaffected by aromatase inhibition. Together, these results suggest a role for estrogens during the initial growth phase of SNB development. In this study, we tested whether ovarian hormones could support SNB somal and dendritic development. Motoneuron morphology was assessed in normal males and in females perinatally masculinized with dihydrotestosterone and then either ovariectomized or left intact. SNB motoneurons were retrogradely labeled with cholera toxin-HRP at 4 or 7 weeks of age and reconstructed in three dimensions. Initial growth of SNB dendrites was reduced after ovariectomy in masculinized females. However, no differences in dendritic length were seen at 7 weeks of age between intact and ovariectomized masculinized females, and lengths in both groups were significantly lower than those of normal males. Together with previous findings, these results suggest that estrogens are involved in the early growth of SNB dendrites, but not in their subsequent retraction.     

Biomarkers of free radical injury during spinal cord ischemia.

Plasma and urinary levels of 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) were analysed at baseline and during the ischemia-reperfusion period in experimental spinal cord ischemia. A significant and immediate increase of 8-iso-PGF(2alpha) in plasma at the start and up to 60 min, and in the urine at 90-150 min following ischemia indicate an association of oxidative injury. The inflammatory response indicator 15-keto-dihydro-PGF(2alpha) in plasma increased significantly at the start and up to 60 min after ischemia. No such increase was seen in animals with no spinal cord ischemia. Thus, free radical mediated and cyclooxygenase catalysed products of arachidonic acid are increased during spinal cord ischemia as a consequence of oxidative injury and inflammation.     

Stimulation of Antioxidant Enzymes and Lipid Peroxidation by UV-B Irradiation in Thylakoid Membranes of Wheat

In wheat seedlings (Triticum aestivum L. cv. 2329) oxidative stress caused by UV-B radiation led to lipid peroxidation of thylakoid membrane; it was expressed in term of malondialdehyde (MDA) formation. The peroxidation of lipids of thylakoid membrane in isolated chloroplasts was prevented when flavonoids quercetin and rutin were supplied into the incubation medium. The activities of superoxide dismutase, ascorbate peroxidase, and catalase increased during the first hours of UV-B exposure. A comparative study of UV-B and temperature effects showed different profiles of the antioxidant enzymes and MDA, suggesting that these two stresses have distinct sites of action. In addition to quantitative increase in flavonoids, qualitative change in flavonoid composition was also marked during UV-B stress, and a new peak at 330 nm was found as compared to control. This revised version was published online in July 2006 with corrections to the Cover Date.     

Degradation of mutagens from pyrolysates of tryptophan, glutamic acid and globulin by myeloperoxidase.

Mutagenic compounds isolated from pyrolysates of tryptophan, glutamic acid and globulin were broken down by myeloperoxidase and hydrogen peroxide with loss of their mutagenicity toward Salmonella typhimurium TA98. Lactoperoxidase and horseradish peroxidase were as effective as myeloperoxidase in degradation of the mutagens.     

Transformation of malaria parasites by the spontaneous uptake and expression of DNA from human erythrocytes

The uptake and expression of extracellular DNA has been established as a mechanism for horizontal transfer of genes between bacterial species. Such transfer can support acquisition of advantageous elements, including determinants that affect the interactions between infectious organisms and their hosts. Here we show that erythrocyte-stage Plasmodium falciparum malaria parasites spontaneously take up DNA from the host cell cytoplasm into their nuclei. We have exploited this finding to produce levels of reporter expression in P.falciparum that are substantially improved over those obtained by electroporation protocols currently used to transfect malaria parasites. Parasites were transformed to a drug-resistant state when placed into cell culture with erythrocytes containing a plasmid encoding the human dihydrofolate reductase sequence. The findings reported here suggest that the malaria genome may be continually exposed to exogenous DNA from residual nuclear material in host erythrocytes.