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Results for “Pentachlorophenol”

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PubMed1985

The effects of pentachlorophenol, phenol and other pollutants on the liver of carp (Cyprinus carpio L.).

Liver tissue of carp was kept in roller tubes and the basal and epinephrine-induced release of glucose after 6 or 24 hr incubation were measured. The amount of liver glycogen after incubation was also determined. The liver was taken from carp treated in vivo with pollutants, mainly PCP or phenol, or was exposed to these pollutants in vitro. Treatment of carp in vivo with 10-10(4) micrograms/l phenol reduced the basal and the epinephrine-induced release of glucose from the liver. Treatment with low doses increased the glycogen content of the liver slightly, treatment with higher doses reduced the amount. Treatment of carp with low doses of several pollutants decreased mainly the basal glucose release from the liver and reduced the glycogen content. In vitro incubation of the liver with PCP or phenol for 3 days reduced at first the basal release and later the epinephrine-stimulated release of glucose from the liver. After a few days the glycogen content of liver exposed to pollutants was more strongly reduced than that of controls. The phosphorylase activity was slightly increased in liver tissue by the pollutants.

Animals↗
PubMed1990

The effects of pentachlorophenol (PCP) at the toad neuromuscular junction.

1. Effects of PCP at the frog neuromuscular junction were studied in vitro in sciatic nerve sartorius muscle of the toad Pleurodema-thaul. 2. Within the concentration 0.003-0.1 mM, PCP caused a dose-time-dependent block of evoked transmitter release acompanied by an increase in the rate of spontaneous quantal release. 3. PCP induced an increase in miniature endplate potential (MEPP) frequency and it was not antagonized in a Ca2(+)-free medium, indicating that it does not depend upon Ca2+ influx from the external medium, but may act by releasing Ca2+ from intraterminal stores. 4. The present data, together with previous results concerning PCP at eighth sympathetic ganglia indicate that 3,4-diaminopyridine (3,4-DAP) counteracts the effects of PCP on synaptic transmission. This result suggests that PCP interfering Ca2+ influx occurs during depolarization of motor nerve terminals.

4-Aminopyridine↗
PubMed2005

Studies on adsorption, desorption and biodegradation of pentachlorophenol by the anaerobic granular sludge in an upflow anaerobic sludge blanket (UASB) reactor.

PCP-degrading anaerobic granular sludge could be formed in an upflow anaerobic sludge blanket (UASB) reactor that was seeded with anaerobic sludge acclimated to chlorophenol. When hydraulic retention time (HRT) was 20-22 h and PCP loading rate was 200-220 mgL(-1)d(-1), the wastewater containing 170-180 mgL(-1) PCP could be treated effectively in UASB reactor, and PCP removal rate reached up to 99.5%. PCP adsorption and desorption by anaerobic granular sludge follow Freundlich isothermal equation and part of adsorption capacity was not reversible. And the isothermal equation could well describe the variation law of PCP adsorption and desorption by anaerobic granular sludge. The results indicated that the principal removal mechanism of PCP was biodegradation by anaerobic granular sludge, but not adsorption or volatilization.

Adsorption↗
PubMed1997

Induction of glutathione depletion, p53 protein accumulation and cellular transformation by tetrachlorohydroquinone, a toxic metabolite of pentachlorophenol.

Glutathione (GSH) conjugate formation with tetrachlorohydroquione (TCHQ) and the GSH content in vivo were measured by capillary zone electrophoresis. A more than 60% depletion of GSH content was found in liver tissue of mice treated with TCHQ. In addition, p53 protein accumulation and DNA fragmentation was induced by TCHQ. A two-stage model of chemical transformation of mouse embryonic fibroblasts was used to elucidate the transformation activity of TCHQ in vitro, and a 33% foci formation efficiency was found at the concentration of 5 microM. GSH depletion caused by TCHQ could abolish the protective ability of the cell against reactive oxygen species provided by GSH. When DNA was damaged, p53 protein accumulated in the nucleus and, in the case of severe damage, initiated apoptosis. TCHQ's ability to cause GSH depletion and DNA damage may play a role in the cytotoxic and genotoxic properties of its metabolic precursor, PCP.

3T3 Cells↗