Sensitized formation of oxidatively generated damage to cellular DNA by UVA radiation

Cadet, Jean,Douki, Thierry,Ravanata, Jean-Luc,Di Mascio, Paolo Korean Society of Photoscience 2009 Photochemical & photobiological sciences Vol.8 No.7

The survey is aimed at critically reviewing information on the UVA-mediated oxidative reactions to cellular components with emphasis on DNA as the result of mostly photosensitized pathways. It appears clearly that UVA radiation is relatively much more efficient than UVB photons in inducing oxidative processes. The main UVA-induced oxidative degradation pathways of DNA are reported and discussed mechanistically. They are mostly rationalized in terms of a major contribution of singlet molecular oxygen ($^1O_2$) and to a lesser extent of hydroxyl radical (${\cdot}OH$), that in the latter case originates from Fenton-type reactions. This leads to the predominant formation of 8-oxo-7,8-dihydroguanine together with smaller amounts of oxidized pyrimidine bases and DNA strand breaks in UVA-irradiated cells.

The mouse Wnt/PCP protein Vangl2 is necessary for migration of facial branchiomotor neurons, and functions independently of Dishevelled

Glasco, D.M.,Sittaramane, V.,Bryant, W.,Fritzsch, B.,Sawant, A.,Paudyal, A.,Stewart, M.,Andre, P.,Cadete Vilhais-Neto, G.,Yang, Y.,Song, M.R.,Murdoch, J.N.,Chandrasekhar, A. Academic Press 2012 Developmental Biology Vol.369 No.2

During development, facial branchiomotor (FBM) neurons, which innervate muscles in the vertebrate head, migrate caudally and radially within the brainstem to form a motor nucleus at the pial surface. Several components of the Wnt/planar cell polarity (PCP) pathway, including the transmembrane protein Vangl2, regulate caudal migration of FBM neurons in zebrafish, but their roles in neuronal migration in mouse have not been investigated in detail. Therefore, we analyzed FBM neuron migration in mouse looptail (Lp) mutants, in which Vangl2 is inactivated. In Vangl2<SUP>Lp/+</SUP> and Vangl2<SUP>Lp/Lp</SUP> embryos, FBM neurons failed to migrate caudally from rhombomere (r) 4 into r6. Although caudal migration was largely blocked, many FBM neurons underwent normal radial migration to the pial surface of the neural tube. In addition, hindbrain patterning and FBM progenitor specification were intact, and FBM neurons did not transfate into other non-migratory neuron types, indicating a specific effect on caudal migration. Since loss-of-function in some zebrafish Wnt/PCP genes does not affect caudal migration of FBM neurons, we tested whether this was also the case in mouse. Embryos null for Ptk7, a regulator of PCP signaling, had severe defects in caudal migration of FBM neurons. However, FBM neurons migrated normally in Dishevelled (Dvl) ½ double mutants, and in zebrafish embryos with disrupted Dvl signaling, suggesting that Dvl function is essentially dispensable for FBM neuron caudal migration. Consistent with this, loss of Dvl2 function in Vangl2<SUP>Lp/+</SUP> embryos did not exacerbate the Vangl2<SUP>Lp/+</SUP> neuronal migration phenotype. These data indicate that caudal migration of FBM neurons is regulated by multiple components of the Wnt/PCP pathway, but, importantly, may not require Dishevelled function. Interestingly, genetic-interaction experiments suggest that rostral FBM neuron migration, which is normally suppressed, depends upon Dvl function.

Ethylene and mixed 2-butene cis/trans isomers metathesis: Influence of lanthanum as a second metal on the WO3/SiO2 catalysts

Piyasan Praserthdam,Narongrat Poovarawan,Thidaya Thitiapichart,Kongkiat Suriye,Joongjai Panpranot,Wimonrat Limsangkass,Francisco José Cadete Santos Aires 한국화학공학회 2016 Korean Journal of Chemical Engineering Vol.33 No.1

Lanthanum (0.5, 0.6, 0.75, 0.9 and 1 wt%) was added as a second metal on the 9 wt% WO3/SiO2 catalysts by the incipient wetness impregnation method. The catalysts were tested in the metathesis reaction of ethylene and 2- butene using either pure 2% trans-2-butene and the mixture of 1% cis- and 1% trans-2-butene as the reaction feed and were characterized by X-ray diffraction (XRD), nitrogen physisorption (BET), inductively coupled plasma optical emission spectrometry (ICP-OES), scanning electron microscopy, ion-exchange titration, FT-Raman, ammonia temperature programmed desorption (NH3-TPD) and reactant temperature programmed desorption (reactant-TPD). An optimum lanthanum loading at 0.5 wt% could improve dispersion of tungsten active phase and adsorption properties of the reactants on the catalysts. The adsorption of the mixed cis/trans-2-butene isomer was much improved on the La- WO3/SiO2 catalysts with 0.5 wt% La.

Protective potentials of far-infrared ray against neuropsychotoxic conditions

Sharma, Naveen,Shin, Eun-Joo,Kim, Nam Hun,Cho, Eun-Hee,Jeong, Ji Hoon,Jang, Choon-Gon,Nah, Seung-Yeol,Nabeshima, Toshitaka,Yoneda, Yukio,Cadet, Jean Lud,Kim, Hyoung-Chun Elsevier 2019 Neurochemistry International Vol.122 No.-

<P><B>Abstract</B></P> <P>Compelling evidence suggests that far-infrared ray (FIR) possesses beneficial effects on emotional disorders. However, the underlying mechanism conveyed by FIR remains unclear. Recently, we demonstrated that exposure to FIR induces antioxidant potentials via up-regulation of glutathione peroxidase (GPx)-1 gene. The antioxidant potentials might be important for the modulation on the neuropsychotoxic conditions. Exposure to FIR protects from methamphetamine (MA)-induced memory impairments via phosphorylation of ERK <SUB>1/2</SUB> signaling by positive modulation of protein kinase C δ (PKCδ), M1 muscarinic acetylcholine receptor (M1 mAChR), and nuclear factor E2-related factor 2 (Nrf2) transcription factor. In addition, exposure to FIR positively modulates MA-induced behavioral sensitization via attenuating mitochondrial dysfunction by down-regulation of dopamine D1 receptor. In this mini-review, we have discussed with the protective potentials mediated by FIR against MA-induced psychotoxic burdens.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Far-infrared ray (FIR) protects from methamphetamine (MA)-induced psychotoxicity. </LI> <LI> FIR induces antioxidant potentials via up-regulation of glutathione peroxidase-1. </LI> <LI> FIR attenuates MA memory loss via ERK <SUB>1/2</SUB> by modulation of PKCδ, M1 mAChR, and Nrf2. </LI> </UL> </P>

Significance of protein kinase C in the neuropsychotoxicity induced by methamphetamine-like psychostimulants

Shin, Eun-Joo,Dang, Duy-Khanh,Hwang, Young Gwang,Tran, Hai-Quyen,Sharma, Naveen,Jeong, Ji Hoon,Jang, Choon-Gon,Nah, Seung-Yeol,Nabeshima, Toshitaka,Yoneda, Yukio,Cadet, Jean Lud,Kim, Hyoung-Chun Elsevier 2019 Neurochemistry International Vol.124 No.-

<P><B>Abstract</B></P> <P>The abuse of methamphetamine (MA), an amphetamine (AMPH)-type stimulant, has been demonstrated to be associated with various neuropsychotoxicity, including memory impairment, psychiatric morbidity, and dopaminergic toxicity. Compelling evidence from preclinical studies has indicated that protein kinase C (PKC), a large family of serine/threonine protein kinases, plays an important role in MA-induced neuropsychotoxicity. PKC-mediated N-terminal phosphorylation of dopamine transporter has been identified as one of the prerequisites for MA-induced synaptic dopamine release. Consistently, it has been shown that PKC is involved in MA (or AMPH)-induced memory impairment and mania-like behaviors as well as MA drug dependence. Direct or indirect regulation of factors related to neuronal plasticity seemed to be critical for these actions of PKC. In addition, PKC-mediated mitochondrial dysfunction, oxidative stress or impaired antioxidant defense system has been suggested to play a role in psychiatric and cognitive disturbance induced by MA (or AMPH). In MA-induced dopaminergic toxicity, particularly PKCδ has been shown to trigger oxidative stress, mitochondrial dysfunction, pro-apoptotic changes, and neuroinflammation. Importantly, PKCδ may be a key mediator in the positive feedback loop composed of these detrimental events to potentiate MA-induced dopaminergic toxicity. This review outlines the role of PKC and its individual isozymes in MA-induced neuropsychotoxicity. Better understanding on the molecular mechanism of PKCs might provide a great insight for the development of potential therapeutic or preventive candidates for MA (or AMPH)-associated neuropsychotoxicity.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PKC is crucial for the drug dependence induced by MA-like psychostimulants. </LI> <LI> PKC plays a role in the synaptic disturbance and memory impairment induced by MA. </LI> <LI> PKC is involved in the mania-like behaviors induced by MA-like psychostimulants. </LI> <LI> PKCδ mediates and facilitates dopaminergic neurotoxicity induced by MA. </LI> </UL> </P>