19 research outputs found
Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation
The effect of prenatal lead acetate exposure
was studied microscopically together with the
concentration of lead and lipid fluorescent products
(LFP) in the brain of rat fetuses. Wistar rats were
intoxicated with a lead solution containing either 160 or
320 ppm of lead acetate solution during 21 days through
drinking water. The control group (ten rats) received
deionized water for the same period. The rats were killed
on gestation day 21 and fetuses were obtained; the
placenta, umbilical cord and parietal cortex (Cx),
striatum (St), thalamus (Th) and cerebellum (Ce) were
collected for measuring tissue lead concentration, LFP as
an index of lipid peroxidation and histopathologic
examination. Lead contents were increased in placenta,
umbilical cord, St, Th and Cx in both lead-exposed
groups. Lead exposure increased (LFP) in placenta and
umbilical cord, St, Th and Ce as compared to the control
group. Histopathological examination showed severe
vascular congestion in placenta, the Cx, St, Th and Ce
with hyperchromatic and shrunken cells. Interstitial
oedema was found in all regions studied of both lead
exposed groups. The morphometric evaluation of the
studied brain regions showed an absolute decrease in
total cell number and increased number of damaged cells and interstitial oedema. Our results show that
morphological changes in rat brain are correlated with
increased lipid peroxidation, and the lead levels of the
umbilical cord, however it is not clear whether oxidative
stress is the cause or the consequence of these
neurotoxic effects of lead
Variability of current clinical practices for locally advanced cervical cancer through assessment of contouring, prescription, and IMRT/VMAT planning abilities
Q1Q1Revista Internacional - IndexadaA1S
Memory for facial expressions in patients with temporal lobe epilepsy: Preliminary findings
The response of liver lipid peroxidative and antioxidant defense systems of protein undernourished rats to liver regeneration
Regulating Bioactivity of Cu2+ Bis-1,10-phenanthroline Artificial Metallonucleases with Sterically Functionalized Pendant Carboxylates
A novel Osmium-based compound targets the mitochondria and triggers ROS-dependent apoptosis in colon carcinoma
Engagement of the mitochondrial-death amplification pathway is an essential component in chemotherapeutic execution of cancer cells. Therefore, identification of mitochondria-targeting agents has become an attractive avenue for novel drug discovery. Here, we report the anticancer activity of a novel Osmium-based organometallic compound (hereafter named Os) on different colorectal carcinoma cell lines. HCT116 cell line was highly sensitive to Os and displayed characteristic features of autophagy and apoptosis; however, inhibition of autophagy did not rescue cell death unlike the pan-caspase inhibitor z-VADfmk. Furthermore, Os significantly altered mitochondrial morphology, disrupted electron transport flux, decreased mitochondrial transmembrane potential and ATP levels, and triggered a significant increase in reactive oxygen species (ROS) production. Interestingly, the sensitivity of cell lines to Os was linked to its ability to induce mitochondrial ROS production (HCT116 and RKO) as HT29 and SW620 cell lines that failed to show an increase in ROS were resistant to the death-inducing activity of Os. Finally, intra-peritoneal injections of Os significantly inhibited tumor formation in a murine model of HCT116 carcinogenesis, and pretreatment with Os significantly enhanced tumor cell sensitivity to cisplatin and doxorubicin. These data highlight the mitochondria-targeting activity of this novel compound with potent anticancer effect in vitro and in vivo, which could have potential implications for strategic therapeutic drug design. © 2013 Macmillan Publishers Limited All rights reserved