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At least 19 recordsLinked to original sources
PubMed2001

Similarity of an Aroclor-based and a full congener-based method in determining total PCBs and a modeling approach to estimate Aroclor speciation from congener-specific PCB data.

Polychlorinated biphenyls (PCBs) have entered the environment in North America as Aroclor technical mixtures. Most methods used for the determination of total PCB levels in environmental samples visually match patterns of sample peaks to those in Aroclor standards. Concern over the accuracy of Aroclor-based measurements on compositionally modified samples coupled with advancements in analytical techniques have led to congener-specific PCB analysis. In this study, the PCB data from 27 tissue samples determined by an Aroclor-based method and a full congener method were compared in terms of total PCB concentration to assess the reliability of this Aroclor technique for total PCB determination. Our data show a strong correlation between the sum of Aroclors and the total PCBs obtained from the full congener determinations. We also developed a model using the compositional data from three Aroclors (1242, 1254, and 1260) to determine the amount of compositional alteration from original Aroclor patterns in environmental samples. Full congener data, from a variety of tissue types and trophic levels, examined using this method showed that compositional modification from original Aroclor patterns increases with trophic level, with the greatest modification observed in seal and killer whale samples. This result agrees both with expectation and with what has been found in other studies. Such techniques, which connect congener-specific PCB data to Aroclor contamination, may prove useful to investigations into environmental and metabolic fate and transfer processes.

Algorithms↗
PubMed1979

Comparison of the compositions of Aroclor 1242 and Aroclor 1016.

The complete polychlorinated biphenyl compositions of two American products, Aroclor 1242 and its more modern replacement, Aroclor 1016, have been determined by gas-liquid chromatography (GLC) on twelve liquid phases of differing selectivities. Attempts were made to determine the degree of contamination of these Aroclors with chlorinated naphthalenes, using GLC with multiple ion-monitoring mass spectrometry. Chlorinated dibenzofurans, indetectable in Aroclor 1016, were tentatively identified by negative chemical-ionization mass spectrometry and their retention times relative to dieldrin on two GLC liquid phases. Quantitation of the dibenzofurans was initially accomplished using an electron-capture detector, and confirmed by negative chemical-ionization mass spectrometry. Aroclor 1242 contained less than 0.05 mol.% chloronaphthalenes, while Aroclor 1016 contained less than 0.06 mol.% of these compounds. Aroclor 1242 had approximately 150 ppb of chlorinated dibenzofurans, of which 43% was the toxic 2,3,7,8-tetrachloro isomer.

Aroclors↗
PubMed2003

Differential expression of CYP1A1 mRNA in gill, intestine and liver of tilapia fed with PCB Aroclor-1254 and Aroclor-1260 spiked food.

The differential expression of cytochrome P4501A1 gene expression (CYP1A1) in liver, intestine and gill of juvenile tilapia following oral exposure to polychlorinated biphenyl (PCB) Aroclor-1254 or Aroclor-1260 spiked food were investigated. The fish was fed with 0.1 g/g of body weight each day of the spiked food with a concentration of approximately 8 ppm. Fish fed with betaNF- or acetone-spiked food were used as positive and negative controls, respectively. On day 1, 3 and 7 of post-treatment, the fish were sampled and analyzed for the total accumulated levels of PCBs, as well as the induced levels of CYP1A1 mRNA. Our results indicated that the fish fed with PCBs-spiked food showed a time-dependent bioaccumulation of PCBs. The time course studies also revealed that in the first 3 days of feeding, significant increases in CYP1A1 were found in intestine (betaNF: 320% and Aroclor-1260: 290%), followed by liver (betaNF: 144%, Aroclor-1260: 123% and Aroclor-1254: 110%). The transcript levels, then declined slowly. There was no induction of gill CYP1A1 mRNA expression in all treatment groups. Among all the tested tissues, the highest intestinal CYP1A1 transcripts induction has highlighted its prompt response to dietary PCBs exposure. Our study supported the important role of intestine in response to dietary PCBs exposure. In addition, in the present study the relative potency of Aroclor-1260 over Aroclor-1254 in stimulating CYP1A1 expression was discussed, indicating that the highly chlorinated PCBs had a higher potency of bioaccumulation and CYP1A1 mRNA induction.

Animals↗
PubMed2003

Exposure and time dependent DNA strand breakage in hepatopancreas of green-lipped mussels (Perna viridis) exposed to Aroclor 1254, and mixtures of B[a]P and Aroclor 1254.

Green-lipped mussels (Perna viridis) were exposed to Aroclor 1254 (0.5, 5 and 50 microgl(-1)) and a mixture of benzo[a]pyrene (B[a]P) and Aroclor 1254 (0.3+0.5 and 3+5 microgl(-1)) for 12 days. On day 0, 1, 3, 6 and 12, the levels of DNA strand breaks in the mussel hepatopancreas were monitored using an alkaline unwinding assay. The results were compared to the findings of a previous study in which the levels of DNA strand breakage in the same species were measured following exposure to various concentrations of B[a]P (0.3, 3 and 30 microgl(-1)). The results indicated that Aroclor 1254 at a concentration </=50 microgl(-1) did not cause any increase in DNA strand breaks while B[a]P at concentrations ranging from 0.3 to 3 microgl(-1) caused an increase in strand breaks after one day of exposure, followed by an apparent rapid recovery. In contrast, exposure to 30 microgl(-1) B[a]P caused no increase in DNA strand breaks over the exposure period. This was postulated to be due to an early elicitation of the DNA repair system by the relatively high exposure level of B[a]P. This hypothesis was tested in the present study, and the results suggest that exposure to the high B[a]P concentration might have elicited the defense mechanism within the mussels, resulting in no observed increase in DNA strand breaks. An increase in strand breaks was, however, evident when the mussels were exposed to lower B[a]P levels. The levels of DNA strand breaks were correlated with the body burden of B[a]P and Aroclor 1254 but no significant relationship was observed, possibly owing to the rapid metabolism of the toxicant and/or an effective DNA repair mechanism. As a result, DNA strand breakage in the hepatopancreas of green-lipped mussels may not be a suitable biomarker of exposure to the above toxicants in the marine environment. Our findings also suggest that it would be instructive to investigate (1) the role of DNA repair enzymes in the exposed mussels; and (2) the correlation between the activity of these enzymes and the body burden of specific toxicants.

Analysis of Variance↗
PubMed1987

Induction of the hepatic mixed-function oxidases by Aroclor 1254 in the hamster: comparison of Aroclor-induced rat and hamster preparations in the activation of pre-carcinogens in the Ames test.

Hepatic microsomal mixed-function oxidase activities and the metabolic activation of chemical carcinogens to mutagens in the Ames test were investigated using Aroclor 1254-induced rat and hamster preparations. Benzphetamine N-demethylase, NADPH-cytochrome c reductase and cytochromes P-450 and b5 were induced in both animals to the same extent by pre-treatment with Aroclor. However, the O-deethylation of ethoxyresorufin was markedly induced in the rat (147-fold) but only modestly in the hamster (3-fold). 1,2-Benzanthracene and 4-aminobiphenyl were more efficiently activated by the rat preparations while, in contrast, 2-acetylaminofluorene, 2-aminoanthracene, nitrosopiperidine, nitrosopyrrolidine, cyclophosphamide and phenacetin were more efficiently activated by the hamster preparations. No significant difference was observed in the activation of 3-methylcholanthrene, benzo[a]pyrene and 2-aminofluorene. It is concluded that (a) the hamster is relatively refractive to cytochrome P-448 induction, and (b) Aroclor 1254-induced rat and hamster S9 preparations differ in their ability to convert chemical carcinogens to mutagens in the Ames test.

Animals↗
PubMed1981

Biological activity of technical Aroclor 1254 compared to Aroclor 1254 residues: swine fat residues fed to broiler cockerels.

Fat from Aroclor 1254-treated swine was rendered and incorporated into the diets of broiler chicks for 3-4 weeks. The technical Aroclor 1254 which was fed to the swine was also mixed into control lard for comparison at dietary concentrations of 0.07-9.0 mg/kg. The swine-residue PCB seemed to have a higher proportion of strong microsomal inducers, but the technical PCB was slightly more effective in inducing ethoxy resorufin and p-nitro-anisole (pNA) O-dealkylases than the swine-residue PCB. No overt signs of toxicosis were apparent and none of the diets resulted in changes in growth, relative organ weights, microsomal protein or high affinity pNA O-dealkylase. Increases in cytochrome(s) P-450 were significant only at the higher dietary concentrations (approx. 9 mg/kg) while ethoxyresorufin O-dealkylase was induced at dietary concentrations below 1 mg/kg.

Adipose Tissue↗
PubMed1983

Hepatic microsomal O-de-ethylases in cod (Gadus morhua): their induction by Aroclor 1254 but not by Aroclor 1016.

1. The characteristics of hepatic ethoxycoumarin and ethoxyresorufin O-de-ethylases in juvenile cod (Gadus morhua) from the North Sea are described. 2. Feeding Aroclor 1254 to juvenile cod to produce liver concentrations of approx 900 microgram X g-1 (wet wt) induced ethoxycoumarin O-de-ethylase approx 30-fold, but had no effect on ethoxyresorufin O-deethylase activity. 3. Feeding Aroclor 1016 to juvenile cod to produce liver concentrations of approx 300 micrograms X g-1 (wet wt.) did not induce ethoxycoumarin O-de-ethylase activity.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1981

Promoting effects of polychlorinated biphenyls (Aroclor 1254) and polychlorinated dibenzofuran-free Aroclor 1254 on diethylnitrosamine-induced tumorigenesis in the rat.

The hepatic tumor-promoting activity of a commercial polychlorinated biphenyl mixture, Aroclor 1254 (AR 1254), with and without its intrinsic polychlorinated dibenzofuran (PCDF) impurities, was investigated. Male Sprague-Dawley non-inbred albino rats were treated with 66 microgram diethylnitrosamine (DENA)/ml drinking water for 5 weeks and subsequently given a control diet or a diet supplemented (100 ppm for 18 wk) with either AR 1254 or AR 1254 from which the PCDF moieties were removed (AR 1254-PCDF). Of those animals receiving DENA alone, 16% exhibited hepatocellular carcinomas. Of those rats treated with DENA followed by administration of AR 1254 or AR 1254-PCDF, 64 or 84%, respectively, developed hepatocellular carcinomas. Thus promotion with either AR 1254 or AR 1254-PCDF significantly (P less than 0.05) increased the incidence of DENA-initiated hepatocellular carcinomas. Administration of AR 1254 or AR 1254-PCDF alone did not induce hepatic tumors. Therefore, PCDF impurities were not necessary for the promoting activity of AR 1254.

Animals↗
PubMed2001

Effects of continuous and intermittent exposure of lactating mothers to aroclor 1242 on testicular steroidogenic function in the adult male offspring.

Polychlorinated biphenyls (PCBs) are worldwide pollutants and have caused hazardous effects on many animal species including humans. They have been detected in human milk and therefore exposure of newborns to PCBs is unavoidable if they are breast-fed. We present our findings on two experiments performed to test the effects of intermittent and continuous exposure of lactating rats to two different doses (80 microg and 8 microg) of Aroclor 1242 (a PCB congener) on testicular steroidogenic function of their adult male offspring. In experiment I, three groups of lactating dams received daily subcutaneous (SC) injections of either corn oil, 80 microg of Aroclor 1242 and 8 microg of Aroclor 1242 in corn oil, respectively. In experiment II, three groups of lactating dams received two SC injections per week of either corn oil or Aroclor 1242 (80 microg and 8 microg) in corn oil, respectively. Pups in all groups (n=8 per group) were weaned at day 21 and were raised on a normal diet until sacrificed at 90 days. Experiment I: Leydig cell number per testis was significantly (P<0.05) increased and the average volume of a Leydig cell was significantly (P<0.05) reduced in both groups of Aroclor-exposed rats compared to corn oil controls. Both doses of Aroclor resulted in reduced (P<0.05) serum testosterone levels compared to corn oil-treated controls. LH-stimulated testosterone production per testis and per Leydig cell was lower in Aroclor-exposed rats compared to controls. Experiment II: No changes were observed in Leydig cell size and number per testis among the three groups. Serum LH, testosterone and LH-stimulated testicular testosterone production in offspring rats of Aroclor-treated dams were not significantly different (P>.05) from the offspring of corn oil-treated dams. However, these parameters were lower in value in the offspring of dams treated with Aroclor 80 microg compared to the other two groups. LH-stimulated testosterone secretory capacity per Leydig cell was significantly lower in offspring of dams treated with Aroclor compared to controls. Serum T4 and T3 levels were not significantly different among the Aroclor-exposed and control rats in both experiments. These results demonstrate that continuous exposure of lactating mothers to 8 and 80 microg of Aroclor 1242 causes hypotrophy and malfunctioning of Leydig cells in the adult male offspring resulting in a hypoandrogenic status. Intermittent treatment of lactating mothers with 80 microg of Aroclor (but not with 8 microg of Aroclor) also produced malfunctioning of Leydig cells and a hypoandrogenic status in the absence of Leydig cell hypotrophy. However, the Aroclor 8 microg dose was ineffective to produce the above effects.

Age Factors↗
PubMed1980

Polychlorinated biphenyls (Aroclors 1016 and 1242): effects on survival and reproduction in mink and ferrets.

Diets that contained various levels of supplemental Aroclor 1242 or Aroclor 1016 were fed to mink and ferrets to investigate the chronic toxicity of these PCBs in two closely related species. In mink, Aroclor 1242 was found to be more toxic than comparable or higher levels of Aroclor 1016. The Aroclor 1242 diets caused complete reproductive failure at levels as low as five ppm of the diet. Aroclor 1016 impaired reproduction less than Aroclor 1242. Although fewer females whelped and the four-week kit weights were less than the control animals, no outward signs of abnormalities beyond their smaller size were found in the kits whelped and nursed by dams fed Aroclor 1016. Ferrets were more resistant to the effects of either PCB mixture than were the mink, as noted by the lower mortality rate on the Aroclor 1242 diet and the almost normal level of reproduction on the Aroclor 1016 diet. Feeding Aroclor 1242 at 20 ppm resulted in complete reproductive failure, but was not fatal to adult ferrets. This finding is in sharp contrast to the 100% mortality of adult mink fed the same level. Although the chlorine content is similar in both compounds, Aroclor 1242 has a higher percentage of molecules with five or more chlorines per biphenyl. This difference in higher substituted biphenyl isomer content and/or the reduced levels of contaminants in the Aroclor 1016 mixture may be of major importance in evaluating the toxicity of these compounds.

Animals↗
PubMed1983

In vitro cytotoxicity of polychlorinated biphenyls (Aroclors 1016, 1242, 1254 and 1260) and their effect on phospholipid and neutral lipid composition of Chinese hamster ovary (CHO-K1) cells.

Cytotoxicity of 4 Aroclors (1016, 1242, 1254 and 1260) was compared in Chinese hamster ovary (CHO-K1) cells in Ham's F-12 medium. When parameters of toxicity were cell numbers or tissue protein, 50% lethality occurred at Aroclor concentrations between 30 and 45 ppm. An in vitro clonal assay with CHO-K1 cells was a sensitive indicator of cytotoxicity of the polychlorinated biphenyls (PCBs). From EC50 values (concentration that allowed 50% survival of formed colonies), cytotoxicity was lower with Aroclor 1016 (32 ppm) and higher with Aroclors 1254 (27 ppm) and 1260 (28 ppm). In cells exposed 24 h to a marginally cytotoxic dose (20 ppm) of each Aroclor, phospholipid (PL) thin-layer chromatography (TLC) showed an increase in phosphatidylcholine (PC) and a decrease in phosphatidylethanolamine (PE) and diphosphatidylglycerol (DPG). Neutral lipid (NL) TLC of cells given Aroclors 1242, 1254 or 1260 showed a 3-4-fold increase in triglyceride (TG) and a similar reduction in cholesteryl esters (CE); in contrast to Aroclor 1016 which produced no change in TG and a smaller (2-fold) reduction in CE. Cholesterol and free fatty acid fractions were unaffected by any of the Aroclors. The TG:PL ratio remained unchanged in cells given Aroclor 1016, but increased 3-4-fold with Aroclors 1242, 1254, or 1260. Compared to total values in the untreated controls, CHO-K1 cells contained less neutral lipid and more phospholipid only with Aroclor 1016. These results support the concept that differences in the behavior of Aroclor 1016 are related to its PCB composition. Changes in membrane PL and NL components, observed at marginally cytotoxic levels of each Aroclor, provided further evidence that the PCBs may affect membrane integrity and associated metabolic functions.

Animals↗
PubMedDate not supplied

Comparison of the effects of acute and subchronic administration of Aroclor 1254, a commercial mixture of polychlorinated biphenyls, on pentobarbital-induced sleep time and [14C]pentobarbital disposition in mice.

We have reported previously that polychlorinated biphenyls (PCBs) alter neurochemistry and suppress spontaneous locomotor activity in mice. The present study was initiated to determine whether orally administered (Aroclor 1254) would potentiate pentobarbital-induced sleep time. Sleep time was enhanced significantly by Aroclor 1254 (500 mg/kg) given 0 to 8 h prior to pentobarbital, with the peak effect occurring at 2 h. This effect was demonstrated to be dose-responsive in the range of 5 to 25 mg/kg given 2 h prior to pentobarbital, but only slightly larger increments in sleep time were observed with higher doses of PCBs (50, 100, 250, and 500 mg/kg). Administration of vehicle or Aroclor 1254 (30 or 100 mg/kg) for 14 successive days reduced sleep time when pentobarbital was given 45 min after the last dose of vehicle or Aroclor 1254, with a further reduction when pentobarbital was given 24 h after the last dose. As a correlate to the sleep-time studies, levels of pentobarbital and metabolites were measured in brain, liver, and plasma of mice that had received varying doses of Aroclor 1254 2 h prior to [14C]pentobarbital. Elevated levels of pentobarbital and decreased levels of metabolites were found after acute administration of Aroclor 1254 during a period of time when Aroclor 1254-treated mice were still asleep. These effects of Aroclor 1254 on pentobarbital disposition were found to be dose-dependent. Brain levels of pentobarbital in mice after 14 d of Aroclor 1254 treatment (30 mg/kg) were less than those in vehicle-treated animals, and these levels were consistent with the reduced sleep times. Thus, a correlation between pentobarbital brain levels and sleep time in both Aroclor 1254-treated and nontreated animals suggests that Aroclor 1254 does not alter pentobarbital narcosis by a direct action on the brain. Rather, acutely administered Aroclor 1254 may be augmenting sleep time by competing with pentobarbital for metabolic sites in the liver, while chronically administered Aroclor 1254 induces pentobarbital metabolism.

Animals↗
PubMed1998

Comparative carcinogenicity in Sprague-Dawley rats of the polychlorinated biphenyl mixtures Aroclors 1016, 1242, 1254, and 1260.

A comprehensive chronic toxicity and carcinogenicity study was conducted on a series of Aroclors (1016, 1242, 1254, and 1260). Each Aroclor was assessed at multiple dietary concentrations, ranging from 25 to 200 ppm, for 24 months in male and female Sprague-Dawley rats. Liver toxicity was indicated by elevated serum enzyme activity (AST, ALT, and GGT), elevated serum cholesterol concentration, decreases in hematologic parameters (RBC, Hb, and Hct), hepatocellular hypertrophy, an increased incidence of altered hepatocellular foci, and an increased incidence of hepatocellular neoplasms (primarily adenomas). Liver toxicity was distinctly more severe in females than in males. The incidence of hepatocellular neoplasms was highly sex-dependent (females >> males), differed between Aroclor mixtures and, for females, increased with dose and followed the general incidence pattern of Aroclor 1254 > Aroclor 1260 approximately Aroclor 1242 > Aroclor 1016. A significant response (p < 0.05) in males was seen only for the high dose of Aroclor 1260. A small increase in the incidence of thyroid gland follicular cell adenomas was noted in males for Aroclors 1242, 1254, and 1260, with the incidence being uniform across dose groups and Aroclor mixtures. For females, increased survival relative to controls was observed for all Aroclor treatment groups. A significantly decreased trend in the incidence of mammary gland neoplasms compared to control was also noted for females receiving Aroclors 1242, 1254, and 1260.

Animals↗
PubMed1987

Aroclor 1254 as a 2,3,7,8-tetrachlorodibenzo-p-dioxin antagonist: effects on enzyme induction and immunotoxicity.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Aroclor 1254 induced the cytochrome P-450 dependent monooxygenases, aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin O-deethylase (EROD) in rat hepatoma H-4-II E cells and C57BL/6J mice. It has been proposed that both Aroclor 1254 and 2,3,7,8-TCDD induce these enzymes via a common mechanism which features initial binding to the aryl hydrocarbon (Ah) cytosolic receptor protein. The major difference between these compounds was the relative potency (i.e. 2,3,7,8-TCDD much greater than Aroclor 1254). Cotreatment of rat hepatoma H-4-II E cells or C57BL/6J mice with a dose of 2,3,7,8-TCDD which submaximally induces AHH and EROD and a dose of Aroclor 1254 which exhibited little or no induction activity resulted in significant antagonism of the induction effects of 2,3,7,8-TCDD. For example, cotreatment of C57BL/6J mice with 2,3,7,8-TCDD (15 nmol/kg) and Aroclor 1254 (25, 75 and 150 mumol/kg) resulted in up to 23% antagonism of AHH induction by 2,3,7,8-TCDD. Moreover, cotreatment with a higher dose of the 2,3,7,8-TCDD agonist (30 or 50 nmol/kg) partially reversed some of the antagonism by Aroclor 1254. In vivo antagonism was observed only at Aroclor 1254/2,3,7,8-TCDD molar ratios of 1667:1, 5000:1 and 10,000:1. Administration of 2,3,7,8-TCDD (3.72 nmol/kg) to C57BL/6J mice resulted in a 76% decrease in the splenic plaque forming cell response to sheep red blood cells. This T-cell mediated immunotoxic effect of 2,3,7,8-TCDD segregates with the Ah locus. In contrast, administration of 5, 15, 75 and 150 mumol/kg of Aroclor 1254 resulted in impairment of the immune response only at the highest dose level. However, cotreatment of mice with 2,3,7,8-TCDD (3.72 nmol/kg) and Aroclor 1254 (5, 15 or 75 mumol/kg) resulted in no significant decrease in the plaque forming cell response and complete protection from the immunotoxicity of 2,3,7,8-TCDD. Cotreatment of the mice with Aroclor 1254 (75 mumol/kg) and a higher dose of the 2,3,7,8-TCDD agonist resulted in partial reversal of the protective effects of Aroclor 1254. The in vitro and in vivo data suggest that within specific antagonist/agonist dose ratios, Aroclor 1254 can antagonize at least 2 Ah receptor-mediated effects of 2,3,7,8-TCDD, namely AHH induction and immunotoxicity.

Animals↗