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Biomedical subjects

P Sheng

Publications and source records attributed to P Sheng.

At least 37 records · Page 2Linked to original sources
PubMed1996

AP-1 DNA-binding activation by methamphetamine involves oxidative stress.

Methamphetamine (METH) caused dose-dependent increases in AP-1 DNA-binding activity in both nontransgenic (Non-Tg) and CuZn-SOD transgenic (SOD-Tg) mice. However, the increases in SOD-Tg mice were less prominent than those observed in Non-Tg animals. The time-course of METH-induced AP-1 changes was similar in both strains of mice. AP-1 binding activity showed an initial increase at 1 h, peaked at 3 h, and then gradually declined. AP-1 binding activity was back to normal by the 72-h time point. Regional analyses of METH effects revealed increases in the caudate putamen and cerebellum, with the striatum showing relatively higher METH-induced AP-1 DNA-binding activation. These regional effects were also attenuated in the SOD-Tg mice. These data indicate that METH-induced stimulation of AP-1 DNA-binding depends on cellular redox status. These results are consistent with in vitro studies that have reported that several transcription factors are regulated through redox mechanisms.

Animals↗
PubMed1996

Methamphetamine-induced neurotoxicity is associated with increased striatal AP-1 DNA-binding activity in mice.

Multiple injections of methamphetamine (METH) produce long-lasting neurotoxic effects on the nigrostriatal dopamine (DA) system. The drug also causes increases in AP-1 DNA-binding activity in mice. In the present study, we tested the idea that toxic doses of METH might cause long-term increases in AP-1 DNA-binding. Mice were given 10 mg/kg of METH 2, 3 or 4 times at a 2 h interval in 1 day. Striatal DA levels were markedly decreased at 3 h and 24 h in all injection groups. After 1 week, striatal DA level recovered to near control in the METH x2 group, but were still significantly decreased in the METH x3 and x4 groups. Similar drug administration schedules caused increases in AP-1 DNA-binding activity at the 3 h time point in all groups. The AP-1-binding activity almost returned back to control level in the x2 and x3 injection groups at the 24 h and 1 week time point, but there were still increased levels of AP-1-binding activity in the METH x4 group. These findings raise the possibility that METH-induced neurotoxicity might involve prolonged activation of AP-1 transcription factor. This might be related to the report that c-fos or c-jun activation may be important in some models of neurodegeneration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Environmental radiation real-time monitoring system permanently installed near Qinshan Nuclear Power Plant.

An environmental radiation real-time monitoring system with high pressure ionization chamber was developed. It has been installed permanently in the vicinity of Qinshan Nuclear Power Plant, the first built in mainland China. The system consists of four basic components: environmental radiation monitors; data communication network; a data processing center; and a remote terminal computer situated in Hangzhou. It has provided five million readings of environmental radiation levels as of January 1993.

Air Pollutants, Radioactive↗
PubMed1995

Involvement of oxidative and L-arginine-NO pathways in the neurotoxicity of drugs of abuse in vitro.

1. Inhibitors of nitric oxide (NO) formation or ADP-ribosylation attenuate methamphetamine (METH)- and methylenedioxymetamphetamine (MDMA)-induced neurotoxicity on dopaminergic and serotonergic cells in primary cultures. 2. They also prevent METH-induced reactive gliosis in dopaminergic cultures. 3. Overexpression of superoxide dismutase (SOD) in cells obtained from SOD-transgenic mice also attenuates drug-induced toxicity. 4. These data indicate a role for oxygen-based and NO free radicals in the mechanisms of cell death associated with drugs of abuse in vitro.

Adenosine Diphosphate Ribose↗
PubMed1994

Methamphetamine (METH) causes reactive gliosis in vitro: attenuation by the ADP-ribosylation (ADPR) inhibitor, benzamide.

We examined the effects of methamphetamine (METH) in an in vitro model of rat fetal mesencephalic cells. METH causes loss of dopamine (DA) cells and neuronal process degeneration. In addition, the drug causes an increase in reactive gliosis as shown by the number of cells that stain for and by the intensity of staining with a glial fibrillary acidic protein (GFAP) antibody. Co-incubation of METH-treated cells with benzamide, which is a known inhibitor of ADP-ribosylation (ADPR), attenuated METH effects on both DA and glial cells. However, the effects of benzamide were somewhat more prominent on the glial cells. These results suggest that ADP-ribosylation may play a very important role in the development of reactive gliosis after the administration of neurotoxic agents.

Adenosine Diphosphate Ribose↗
PubMed1994

Attenuation of methamphetamine-induced neurotoxicity in copper/zinc superoxide dismutase transgenic mice.

Administration of methamphetamine (METH) to rats and nonhuman primates causes loss of terminals in the nigrostriatal dopaminergic system. The mechanism by which METH causes its neurotoxicity is not known. To evaluate further the role of oxyradicals in METH-induced neurotoxicity, we have tested its effects in CuZn superoxide dismutase (SOD) transgenic (Tg) mice, which express the human CuZnSOD gene. In non-Tg mice, acute METH administration causes significant decreases in levels of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striata and cortices of non-Tg mice. In contrast, there were no significant decreases in cortical or striatal DA in the SOD-Tg mice. The effects of METH on DOPAC were also attenuated in both structures of these SOD-Tg mice. Chronic METH administration caused decreases in levels of striatal DA and DOPAC in the non-Tg mice, whereas the SOD-Tg mice were not affected. These results suggest that METH-induced dopaminergic toxicity in mice may be secondary to increased production of reactive oxygen species such as the superoxide radical.

3,4-Dihydroxyphenylacetic Acid↗