23 research outputs found
Environmental sensing and response genes in cnidaria : the chemical defensome in the sea anemone Nematostella vectensis
Author Posting. © The Author(s), 2008. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Cell Biology and Toxicology 24 (2008): 483-502, doi:10.1007/s10565-008-9107-5.The starlet sea anemone Nematostella vectensis has been recently established as a
new model system for the study of the evolution of developmental processes, as cnidaria
occupy a key evolutionary position at the base of the bilateria. Cnidaria play important
roles in estuarine and reef communities, but are exposed to many environmental stressors.
Here I describe the genetic components of a ‘chemical defensome’ in the genome of
N. vectensis, and review cnidarian molecular toxicology. Gene families that defend
against chemical stressors and the transcription factors that regulate these genes have
been termed a ‘chemical defensome,’ and include the cytochromes P450 and other
oxidases, various conjugating enyzymes, the ATP-dependent efflux transporters,
oxidative detoxification proteins, as well as various transcription factors. These genes
account for about 1% (266/27200) of the predicted genes in the sea anemone genome,
similar to the proportion observed in tunicates and humans, but lower than that observed
in sea urchins. While there are comparable numbers of stress-response genes, the stress
sensor genes appear to be reduced in N. vectensis relative to many model protostomes
and deuterostomes. Cnidarian toxicology is understudied, especially given the important
ecological roles of many cnidarian species. New genomic resources should stimulate the
study of chemical stress sensing and response mechanisms in cnidaria, and allow us to
further illuminate the evolution of chemical defense gene networks.WHOI Ocean Life Institute and NIH R01-ES01591
AECHL-1, a novel triterpenoid, targets tumor neo-vasculature and impairs the endothelial cell cytoskeleton
The role of ascorbate in antioxidant protection of biomembranes: Interaction with vitamin E and coenzyme Q
One of the vital roles of ascorbic acid (vitamin C) is to act as an antioxidant to protect cellular components from free radical damage. Ascorbic acid has been shown to scavenge free radicals directly in the aqueous phases of cells and the circulatory system. Ascorbic acid has also been proven to protect membrane and other hydrophobic compartments from such damage by regenerating the antioxidant form of vitamin E. In addition, reduced coenzyme Q, also a resident of hydrophobic compartments, interacts with vitamin E to regenerate its antioxidant form. The mechanism of vitamin C antioxidant function, the myriad of pathologies resulting from its clinical deficiency, and the many health benefits it provides, are reviewed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44796/1/10863_2004_Article_BF00762775.pd
Genotoxicity assessment of the antifungal antibiotic aureofungin in Salmonella typhimurium and Swiss albino mice
Effects of cytochalasins on developing frog embryos: protection with l-cysteine and ?-d-glucosamine
Immunoneutralization of insulin partially modifies dorsoventral patterning in developing frog embryos
Bis(quercetinato)oxovanadium IV Reverses Metabolic Changes in Streptozotocin-Induced Diabetic Mice
Organic vanadium compounds offer several advantages in the treatment of diabetes, yet they are impractical to use because of known side effects. In order to ameliorate the side effects of vanadium, we conjugated it with quercetin to form bis(quercetinato)oxovanadium IV (BQOV). This study evaluates the effect of BQOV treatment on carbohydrate metabolism and overall oxidative stress in streptozotocin-induced (STZ) diabetic mice. Administration of BQOV orally to diabetic mice for 3 weeks led to a reduction of blood glucose levels and the animals exhibited normal glucose tolerance at the end of the study period. The increase in glucose uptake by skeletal muscle and liver as well as the normalization of mRNA levels of G-6-Pase and glucokinase in the liver after BQOV treatment pointed to improvements in carbohydrate metabolism. The analysis of the antioxidant status of serum, liver and pancreas revealed reduced oxidative stress in BQOV-treated animals compared to untreated diabetic controls. Serum analyses for kidney and liver function showed that BQOV treatment provoked total protection of the kidney and partial protection of the liver from diabetogenic insults. The number of insulin-positive cells and the amount of pancreatic insulin in treated mice (1.2038 ± 0.34 ng/mg tissue) did not account for pancreatic regeneration but suggested an insulin-mimetic action on the part of BQOV. Moreover, administration of BQOV for 3 weeks did not show any visible side-effects. This data indicate that BQOV is a safe and potent agent for diabetes treatment, because it is able to improve carbohydrate metabolism and to reduce overall oxidative stress
Differential response of antioxidant defense in HepG2 cells on exposure of Livotrit®, in a concentration dependent manner
Livotrit®, a polyherbal formulation (Zandu, India) is commonly prescribed for liver health. The present study was undertaken to elucidate possible mechanism of antioxidant potential of Livotrit®. Livotrit® exhibited concentration dependent radical scavenging activity, inhibition of lipid peroxidation as well as activation and gene expression of antioxidant enzymes. Interestingly, lower concentration of Livotrit® (0.05%) significantly increased activities and gene expression of catalase, Glutathione reductase (GR) and Gluthathione peroxidase (GPx), while higher concentration of Livotrit® (0.5%) significantly increased antioxidant enzyme Heme-oxygenase 1(HO-1) and not catalase (CAT), GR and GPx. Transcription factor, Nuclear factor erythroid 2-related factor 2 (Nrf2) required for expression of catalase, GR, GPx and HO-1 was efficiently translocated into the nucleus at both concentrations. Inspite of this, concentration dependent activation of these enzymes was found to be mediated through miRNAs involved in regulation of their gene expression. Keywords: Antioxidant enzymes, HO-1, BACH-1, miRN