Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Photocatalysts Pt/TiO2 coated on hollow glass beads were prepared by tetrabutyl titanate hydrolysis with Sodium silicate on hollow glass beads at various condition and loaded with platinum varying from 0.2% to 2.4% by weight. Sodium pentachlorophenolate (PCP-Na) solution were used to examined for their photoactivity and characterized by X-ray and BET. The results indicated that the optimization condition to prepare photocatalysts: Water to titanium alkoxides was 100, Sintering temperature was 650 degrees C, Diameter of hollow glass beads was 0.5 mm, TiO2: sodium silicate: hollow glass beads was 10:2.5:20, Platinum content of photocatalysts was about 1.4%-1.6%. When the experiments were carried out in such conditions, the initial concentration of PCP-Na was 100 mg/L, initial pH was 6.5, oxygen flux was 1.6 mL/s, illumination intensity was 30 kW.m-2, catalysts was 2 g/L, illumination time was 2 hours, respectively. Then the rates removals of PCP-Na could reach 92.0%.
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PMID:[Tetrabutyl titanate hydrolysis prepared TiO2 photocatalysis loaded with platinum technology]. 1198 10

Pentachlorophenol has been used as an herbicide, algicide, defoliant, wood preservative, germicide, fungicide, and molluscicide. Pentachlorophenol was nominated by the National Cancer Institute for carcinogenicity testing based on its widespread use as a wood preservative, potential for entering the environment (pentachlorophenol residues have been found worldwide in soil, water, and air samples; in food products; and in human and animal tissues and body fluids), and likelihood of bioaccumulation in the environment (pentachlorophenol is persistent in soil, having a half-life of up to 5 years). Technical Report No. 349 contains the results of the 2-year studies of pentachlorophenol performed by the NTP with B6C3F1 mice. Male and female F344/N rats were exposed to pentachlorophenol (approximately 99% pure) in feed for 28 days or 2 years. Genetic toxicology studies were conducted in vitro in Salmonella typhimurium and cultured Chinese hamster ovary cells and in vivo in rat and mouse bone marrow cells. 28-DAY STUDY IN RATS: Groups of 10 male and 10 female F344/N rats were given 0, 200, 400, 800, 1,600, or 3,200 ppm pentachlorophenol, equivalent to average daily doses of approximately 20, 40, 75, 150, or 270 mg pentachlorophenol/kg body weight to males and females in feed for 28 days. With the exception of one male and two females exposed to 3,200 ppm, all rats survived until the end of the study. The final mean body weights and body weight gains of male rats exposed to 1,600 or 3,200 ppm and female rats exposed to 400, 800, 1,600, or 3,200 ppm were significantly less than those of the controls; rats exposed to 3,200 ppm lost weight during the study. Feed consumption by 3,200 ppm males was less than that by the control group throughout the study. The absolute and relative liver weights of 400, 800, and 1,600 ppm males and all exposed groups of females were significantly greater than those of the controls. Compared to the control groups, the incidences of minimal to mild hepatocyte degeneration in males and females exposed to 400 ppm or greater and the incidences of centrilobular hepatocyte hypertrophy in the 3,200 ppm groups were increased. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were fed diets containing 200, 400, or 600 ppm pentachlorophenol (equivalent to average daily doses of approximately 10, 20, and 30 mg/kg) for 105 weeks. Stop-exposure groups of 60 male and 60 female rats received 1,000 ppm (equivalent to 60 mg/kg) in feed for 52 weeks, after which animals received undosed feed for the remainder of the 2-year study; 10 male and 10 female control and 1,000 ppm rats were evaluated at 7 months. Survival, Body Weights,and Feed Consumption: In the 2-year study, survival of 600 and 1,000 ppm males was greater than that of the controls. Mean body weights of 400 and 600 ppm males and females were generally less than those of controls. When exposure to pentachlorophenol was discontinued at week 52, mean body weights of 1,000 ppm males and females were 17%% and 22%% lower than those of the respective controls; however, by the end of week 87, the mean body weights were similar to those of the controls. Generally, feed consumption by exposed groups was similar to that by the controls. Pathology Findings: At 2 years, the incidence of malignant mesothelioma originating from the tunica vaginalis was significantly greater in 1,000 ppm males than in the controls, and the incidence exceeded the historical control range. Nasal squamous cell carcinomas were present in one control male, three 200 ppm males, one 400 ppm male, and five 1,000 ppm males at 2 years, and the incidence in 1,000 ppm males exceeded the historical control range. At the 7-month interim evaluation, the incidences of centrilobular hepatocyte hypertrophy in 1,000 ppm males and females and hepatocyte cytoplasmic vacuolization in 1,000 ppm males was significantly greater than those in the controls. At 2 years, the incidences of several nonneoplastic liver lesions including hepatodiaphragmatic nodules and hepatocyte cystic degeneration in all exposed ation in all exposed groups of males and basophilic foci in 1,000 ppm males were increased compared to the controls. GENETIC TOXICOLOGY: Pentachlorophenol (91.6%% pure) was tested in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 at doses up to 30 μg/plate with and without induced rat or hamster liver S9; no significant increases in the number of revertant colonies were observed in any of the strain/activation combinations. When tested for cytogenetic effects in cultured Chinese hamster ovary cells, pentachlorophenol was weakly positive for induction of sister chromatid exchanges and chromosomal aberrations. In the sister chromatid exchange test, a weakly positive response was observed within a concentration range of 3 to 30 μg/mL in the absence of S9; with S9, no induction of sister chromatid exchanges was noted. In the chromosomal aberrations test, pentachlorophenol was negative without S9 but induced small but significant increases in the frequency of aberrant cells in the presence of S9 at doses of 80 and 100 μg/mL. In contrast to the positive in vitro results in the test for induction of chromosomal aberrations, no increase in the frequency of micronucleated erythrocytes was noted in bone marrow of male rats or mice administered pentachlorophenol by intraperitoneal injection three times at 24 hour intervals. The highest dose administered to rats (75 mg/kg) and mice (150 mg/kg) was lethal. CONCLUSIONS: Under the conditions of this 2-year feed study, there was no evidence of carcinogenic activity of pentachlorophenol in male or female F344/N rats fed diets containing 200, 400, or 600 ppm. There was some evidence of carcinogenic activity of pentachlorophenol in male F344/N rats given feed containing 1,000 ppm for 1 year followed by control feed for 1 year (stop-exposure study), based on increased incidences of mesothelioma and nasal squamous cell carcinoma. There was no evidence of carcinogenic activity of pentachlorophenol in female rats given feed containing 1,000 ppm for 1 year and maintained on control feed for 1 year. Stop-exposure males and females recovered from a transitory reduction in body weight gain by the end of the 2-year study, and males had increased survival compared to the controls. Synonyms: Chlorophen; PCP; penchlorol; penta; pentachlorofenol; pentachlorofenolo; 2,3,4,5,6-pentachlorophenol Trade names: Acutox; Chem-Penta; Chem-Tol; Cryptogil ol; Dowicide 7; Dowicide EC-7; Dow Pentachlorophenol DP-2 Antimicrobial; Durotox; EP 30; Fungifen; Fungol; Glazd Penta; Grundier Arbezol Lauxtol; Lauxtol A; Liroprem; Moosuran; Pentacon; Penta-Kil; Pentasol; Penwar; Peratox; Permacide; Permagard; Permasan; Permatox; Priltox; Permite; Santophen; Santophen 20; Sinituho; Term-i-Trol; Thompson's Wood Fix; Weedone; Witophen P
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PMID:NTP Toxicology and Carcinogenesis Studies of Pentachlorophenol (CAS NO. 87-86-5) in F344/N Rats (Feed Studies). 1257 80

Toxicology studies of pentachlorophenol, a biocide used primarily as a wood preservative, were conducted by feeding diets containing a technical-grade composite, Dowicide EC-7 (a technical grade formulation), or pure pentachlorophenol to groups of B6C3F1 mice for 30 days. These three grades plus another commercial grade of pentachlorophenol (DP-2) were used in 6-month studies. These studies were followed by 2-year carcinogenicity studies of technical-grade pentachlorophenol and of Dowicide EC-7 in feed. Genetic toxicology studies were conducted in Salmonella typhimurium and in Chinese hamster ovary (CHO) cells. Thirty-Day and Sixteen-Month Studies: Groups of 19 male mice and 5-15 female mice were fed diets containing 0, 20, 100, 500, 2,500, or 12,500 ppm technical-grade pentachlorophenol, Dowicide EC-7, or pure pentachlorophenol for 30 consecutive days. Necropsies and histopathologic examinations were performed on all animals. Selected organs were weighed. Supplemental analyses included hematology, serum chemistry, urinalysis, immunology, and hepatic enzyme induction. Compound-related deaths were observed at the highest dose (12,500 ppm) with all three materials and at 2,500 ppm with EC-7 and pure pentachlorophenol (males only). Decreases in body weight gain were also observed in the groups in which deaths occurred. Diffuse centrilobular cytomegaly, karyomegaly, nuclear atypia, degeneration, or necrosis of the liver were compound-related lesions observed in all groups that received pure pentachlorophenol, technical-grade pentachlorophenol, or EC-7 at 500 ppm and above. Serum enzymes associated with liver injury were increased. In the 6-month studies, groups of 10 male and 10 female mice were given diets containing the various grades of pentachlorophenol at the following dietary concentrations: 200, 600, or 1,800 ppm technical-grade pentachlorophenol; 200, 600, or 1,200 ppm DP-2 (not used in the 30-day studies); 200, 600, or 1,200 ppm EC-7; or 200, 500, or 1,500 ppm pure pentachlorophenol for 26-27 weeks. Common control groups of 10 male and 10 female mice were fed control diets. Additional groups of male mice were examined for behavioral, histopathologic, clinical pathology, biochemical, and immunologic effects. All mice exposed at the highest dose of technical-grade pentachlorophenol died, as did 2/10 male mice exposed at the highest dose of DP-2. No deaths were observed in mice exposed to EC-7 or pure pentachlorophenol. Markedly lower final body weights were observed in the high dose groups only (all grades of pentachlorophenol). No chemical-relatedclinical signs were observed at sublethal doses. No major behavioral changes were observed after 5 weeks' exposure, but increased motor activity and heightened startle responses were present at the end of the study in female mice exposed to all four grades of pentachlorophenol. All grades of pentachlorophenol caused increases in serum enzymes associated with liver injury. All grades of pentachlorophenol also resulted in a dose-related induction of aryl hydrocarbon hydroxylase and an increase in cytochrome P450. However, the technical grade was a more powerful inducer than the other grades of pentachlorophenol. Pure pentachlorophenol had no effect on humoral or cell-mediated immunity. However, DP-2 and particularly technical-grade pentachlorophenol depressed humoral immune function. A dose-related increase in liver weight was observed in mice exposed to all grades of pentachlorophenol. A dose-related increase in spleen weight was observed in male mice exposed to all grades of pentachlorophenol; a decrease in spleen weight was observed in female mice exposed to all grades of pentachlorophenol except pure. After 6 months' exposure, histopathologic examination consistently revealed effects in the liver and urinary bladder. The liver lesions were present at all doses with all four grades of pentachlorophenol but were less severe at comparable doses in the mice exposed to pure pentachlorophenol; they consisted of hepatocellular karyomegaly, cytomegaly, and degeneration. The changes in the urinary bladder consisted of a brown granular pigment in the cells of the surface epithelium. No inflammation or proliferative response was associated with the pigment. Based primarily on the liver lesions observed in the 6-month studies, diets chosen for the 2-year studies contained 0, 100, or 200 ppm technical-grade pentachlorophenol or 0, 100, 200, or 600 ppm EC-7, fed to groups of 50 male and 50 female mice. DP-2 and pure pentachlorophenol were not chosen for the 2-year studies because of economic considerations and because the clinicopathologic syndrome observed in the 6-month studies was similar to that observed with EC-7. Body Weights and Survival in the Two-Year Studies: Mean body weights of mice exposed to technical-grade pentachlorophenol and EC-7 were comparable to those of controls until weeks 36-82. Thereafter, a 4%-22% dose-related decrease was observed in the mid and high dose mice exposed to EC-7 and in high dose mice exposed totechnical-grade pentachlorophenol. Females were more affected than males. Feed consumption by exposed mice was similar to that by controls. The average daily doses of technical-grade pentachlorophenol were approximately 17-18 or 35 mg/kg compared with 17-18, 34-37, or 114-118 mg/kg of EC-7. Survival of mice did not appear to be affected by exposure to either technical-grade pentachlorophenol or EC-7 at the doses used in these studies. Neoplastic and Nonneoplastic Effects in the Two-Year Studies: The incidences of hepatocellular adenomas and carcinomas were increased (dose related) in male and female mice exposed to either technical-grade pentachlorophenol or EC-7, although the increase was less marked in females exposed to technical-grade pentachlorophenol (adenomas or carcinomas, combined: technical-grade: male-- control, 7/32, 22%; low dose, 26/47, 55%; high dose, 37/48, 77%; female--3/33, 9%; 9/49, 18%; 9/50, 18%; EC-7: male--control, 6/35, 17%; low dose, 19/48, 40%; mid dose, 21/48, 44%; high dose, 34/49, 69%; female-- 1/34, 3%; 4/50, 8%; 6/49, 12%; 31/48, 65%). The incidences of pheochromocytomas in male mice were significantly greater than those in controls for both technical-grade pentachlorophenol (0/31; 10/45, 22%; 23/45, 51%) and EC-7 (1/34, 3%; 4/48, 8%; 21/48, 44%; 45/49, 92%). These neoplasms were also increased in female mice exposed to EC-7 at the highest dose (0/35; 2/49, 4%; 2/46, 4%; 38/49, 78%) but not in those exposed to technical-grade pentachlorophenol (2/33, 6%; 2/48, 4%; 1/49, 2%). Hyperplasia of the adrenal medulla was observed at increased incidences in mice that received either technical-grade pentachlorophenol (male: 1/31; 10/45; female: 0/33; 4/48; 2/49) or EC-7 (male: 1/34; 19/48; 13/48; 1/49; female: 2/35; 1/49; 5/46; 17/49). The incidences of hemangiosarcomas in the spleen and/or liver were significantly greater than those in controls for high dose female mice that received technical-grade pentachlorophenol (0/35; 3/50, 6%; 6/50, 12%) or EC-7 (0/35; 1/50, 2%; 3/50, 6%; 8/49, 16%). Compound-related nonneoplastic lesions occurred in the liver, spleen, and nose in mice exposed to either technical-grade pentachlorophenol or EC-7. The lesions in the liver included dose-related increased incidences of clear cell foci, chronic active inflammation, pigmentation, necrosis, cytomegaly, proliferation of hematopoietic cells, and bile duct hyperplasia. Increased amounts of extramedullary hematopoiesis of the splenic red pulp were observed at increased incidences in dosed male and high dose female mice that received technical-grade pentachlorophenol (male: 5/30; 15/23; 18/46; female: 2/33; 4/13; 11/47). Acutefocal inflammation of the nasal mucosa and focal metaplasia of the olfactory epithelium were observed at increased incidences in high dose mice that received EC-7 (inflammation--male: 4/35; 1/13; 3/16; 47/49; female: 0/35; 0/14; 2/5; 46/48; focal metaplasia-- male: 2/35; 1/13; 2/16; 46/49; female: 1/35; 0/14; 2/5; 45/48) but not in mice exposed to technical-grade pentachlorophenol. Genetic Toxicology: Pentachlorophenol (91.6% pure; equivalent in purity to the technical-grade pentachlorophenol used in the toxicology studies) was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 when tested in the presence or absence of exogenous metabolic activation (S9). In cytogenetic studies with cultured CHO cells, pentachlorophenol produced an increase in chromosomal aberrations in the presence but not the absence of S9 metabolic activation; conversely, sister chromatid exchanges (SCEs) were induced only in the absence of S9. Audit: The data, documents, and pathology materials from the 2-year studies of pentachlorophenol have been audited. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Conclusions: Under the conditions of these 2-year feed studies, there was clear evidence of carcinogenic activity for male B6C3F1 mice fed diets containing technical-grade pentachlorophenol, as shown by increased incidences of adrenal medullary and hepatocellular neoplasms. There was some evidence of carcinogenic activity for female B6C3F1 mice exposed to technical-grade pentachlorophenol, as shown by increased incidences of hemangiosarcomas and hepatocellular neoplasms. There was clear evidence of carcinogenic activity for male B6C3F1 mice exposed to pentachlorophenol, EC-7, as shown by increased incidences of adrenal medullary and hepatocellular neoplasms. There was clear evidence of carcinogenic activity for female B6C3F1 mice exposed to pentachlorophenol, EC-7, as shown by increased incidences of adrenal medullary and hepatocellular neoplasms and hemangiosarcomas. Chemically related increased incidences of nonneoplastic lesions in mice of each sex included hepatocellular cytomegaly, necrosis, inflammation, pigmentation, and clear cell foci and intrahepatic bile duct hyperplasia. Synonyms or Common Names: chlorophen; PCP; penchlorol; penta; pentachlorofenol; pentachlorofenolo; pentachlorphenol; 2,3,4,5,6-pentachlorophenol Trade Names: Acutox; Chem-Penta; Chem-Tol; Cryptogil ol; Dowicide 7; Dowicide EC-7; Dow Pentachlorophenol DP-2 Antimicrobial; Durotox; EP 30; Fungifen; Fungol; Glazd Penta; Grundier Arbezol; Lauxtol; Lauxtol A; Liroprem; Moosuran; Pentacon; Penta-Kil; Pentasol; Penwar; Peratox; Permacide; Permagard; Permasan;Permatox; Priltox; Permite; Santophen; Santophen 20; Sinituho; Term-i-Trol; Thompson's Wood Fix; Weedone; Witophen P
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PMID:NTP Toxicology and Carcinogenesis Studies of Two Pentachlorophenol Technical-Grade Mixtures (CAS No. 87-86-5) in B6C3F1 Mice (Feed Studies). 1270 35

Sodium pentachlorophenate (Na-PCP) has been used in China for years as an molluscacide to kill oncomelania, which is an intermediate host of Schistosome. To evaluate the effects of its long-term successive usage on environment, human exposure and health, studies were carried out in Sichuan, Jiangxi, Jiangsu and Fujian provinces, with a time gap of more than one month between sample collection and last spray of Na-PCP. Results indicated that PCP contents in surface water, soil, sediment, animals and plants were significantly higher in studied areas than in control areas. The daily intake and the content in urine of PCP were also sigificantify higher in studied areas. But, there was no difference on physical and biochemical examinations except that a 22%-28% decrease of blood cholinesterase activity was found in studied areas. The health effect of impurities in Na-PCP, dioxins and furans, was assessed and discussed.
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PMID:[Environmental pollution, human exposure and its health effect of sodium pentachlorophenate in schistosomiasis prevalent area]. 1574 56

Both pentachlorophenol and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) had been studied widely because of their probable anti-estrogenic activity. Sodium pentachlorophenol (PCP-Na), as a industrial product used in many fields, usually contains a trace of TCDD. The aim of this study was to assess the anti-estrogenic effect of PCP-Na in juvenile goldfish (Carassius auratus) hepatocyte cultures using vitellogenin (VTG) as the biomarker. The ID50 of PCP-Na was investigated and then a series of concentrations (0.001-0.5 microg/ml) of PCP-Na were evaluated to estimate the anti-estrogenic activity. Results showed that PCP-Na was cytotoxic for hepatocytes even at very low concentration < 1.21 microg/ml, and it could not induce VTG at any concentrations tested. Since it failed to stimulate VTG production, the possibility of its anti-estrogenic effect was tested, and a well-known anti-estrogenic compound-tamoxifen was used as positive control. PCP-Na caused a reduction in VTG synthesis in juvenile goldfish (Carassius auratus) hepatocytes at concentrations > 0.1 microg/ml when co-exposure with 1 microg/ml 17beta-estradiol (E2), making its anti-estrogenic activity approximately as potent as tamoxifen. Our results indicate that PCP-Na can act as negative modulators of estrogenic function in juvenile goldfish (Carassius auratus) hepatocytes.
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PMID:Assessing the anti-estrogenic activity of sodium pentachlorophenol in primary cultures of juvenile goldfish (Carassius auratus) hepatocytes using vitellogenin as a biomarker. 1729 50

Hydrothermal decomposition of pentachlorophenol (PCP, C6HCl5O), as the probable human carcinogen, was investigated in a tubular reactor under subcritical and supercritical water with sodium hydroxide (NaOH) addition. The experiments were conducted at a temperature range of 300-420 degrees C and a fixed pressure of 25 MPa, with a residence time that ranged from 10 s to 70 s. Under the reaction conditions, the initial PCP concentrations were varied from 0.25 to 1.39 mmol/L and the NaOH concentrations were varied from 2.5 to 25 times of the concentrations of PCP. The result of this study showed that PCP conversion in supercritical water was highly dependent on the reaction temperature, residence time, and NaOH concentration. PCP conversion in subcritical water is, however, only dependent on reaction temperature. NaOH concentration and residence times were found to have little effect on PCP conversion in subcritical condition. It was found that NaOH concentration affected the dechlorinations of PCP in the supercritical water. The intermediates detected were proposed to be tetrachlorophenol and trichlorophenol, respectively.
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PMID:Hydrothermal decomposition of pentachlorophenol in subcritical and supercritical water with sodium hydroxide addition. 1796 37