ABSTRACT
A laboratory study was performed as the basis for a full-scale bioaugmentation project at a site contaminated with chlorinated ethenes. The objectives of this study were to 1) develop a protocol to enrich for a tetrachloroethene (PCE)-dechlorinating culture from waste activated sludge and anaerobic digester biosolids and 2) monitor the survival of fecal coliform bacteria and bacteriophage, which model enteric viruses, during the enrichment process. A culture was enriched in 8 days with the ability to degrade 6-microM PCE to cis-dichloroethene. Using the enrichment protocol in two identical experiments, significant inactivation of fecal coliform bacteria (2 log) and somatic coliphage (0.33 log) was observed in one of the experiments; no inactivation occurred in the second experiment. The number of F-specific coliphage decreased in both experiments (0.87 and 1.26 log inactivation). Despite the decrease in some of the coliform and bacteriophage numbers, the quantity of organisms and phage particles present after enrichment was still high (approximately 7.5 x 10(5) most probable number/L, 6.9 x 10(6) plaque-forming units (PFU)/L, and 3.3 x 10(5) PFU/L, for fecal coliform bacteria, somatic coliphage, and F-specific coliphage, respectively). This may be cause for concern, depending on the current and future groundwater use at or near a site undergoing bioaugmentation with cultures derived from waste activated sludge and anaerobic digester biosolids.
Subject(s)
Bacteriophages/physiology , Enterobacteriaceae/physiology , Sewage/chemistry , Tetrachloroethylene/chemistry , Water Purification/methods , Anaerobiosis , Biodegradation, EnvironmentalABSTRACT
Chloro-containing fatty acids are a major fraction of extractable, organically bound chlorine in fish. It has been suggested that dichloro stearic acid (9,10-dichlorooctadecanoic acid) (C18) is metabolized to dichloro myristic acid (5,6-dichlorotetradecanoic acid) (C14) which accumulates in tissues. Hence, the biological effects of the C18 dichloro fatty acid could be due to formation of the C14 dichloro fatty acid. In this study we have compared the effects of dichloro stearic and dichloro myristic acid on growth of three widely differing cell lines. Both fatty acids inhibited cell growth; however, dichloro myristic acid had a weaker growth inhibitory effect than dichloro stearic acid. Dichloro myristic acid had a biphasic effect (i.e. growth was stimulated at low concentrations, followed by inhibition at higher concentrations) on the growth of human hepatoma cells and immortalized human kidney epithelial cells, but no such effect on human microvascular endothelial cells. The order of potency for growth inhibition by dichloro myristic acid was consistently human hepatoma cells>immortalized human kidney epithelial cells >human microvascular endothelial cells, whereas the relative potency of dichloro stearic acid was variable. Albumin alone stimulated cell growth and had a stronger protective effect against growth inhibition by dichloro myristic acid than against that of dichloro stearic acid. It seems unlikely that a major part of the effect of dichloro stearic acid on cell growth is caused by conversion to dichloro myristic acid.
Subject(s)
Endothelium, Vascular/drug effects , Kidney Neoplasms/drug therapy , Liver Neoplasms/drug therapy , Myristic Acid/pharmacology , Myristic Acids/pharmacology , Stearic Acids/pharmacology , Tumor Cells, Cultured/drug effects , Analysis of Variance , Cell Division/drug effects , Endothelium, Vascular/growth & development , Humans , Myristic Acids/chemical synthesis , Myristic Acids/therapeutic use , Stearic Acids/chemical synthesis , Stearic Acids/therapeutic useABSTRACT
Chlorinated fatty acids represent a major fraction of extractable, organically bound chlorine in fish. After dietary intake such fatty acids may be transferred from the mother to the foetus through the placenta, and via breast milk to the child. In the present work we have studied the effect of chlorinated oleic acid on the growth of three widely differing types of cells in culture. Chlorinated oleic acid inhibited growth of Human Microvascular Endothelial Cells (HMVEC), Immortilized Human Kidney Epithelial (IHKE) cells, and human Hepatoma cells (HepG2). The order of potency was: HMVEC > IHKE > HepG2. Vitamin E counteracted the inhibitory effect of chlorinated oleic acid on HepG2 cells, but did not significantly affect the fatty acid effect on HMVEC or IHKE. Defatted serum albumin stimulated the growth of HMVEC and IHKE. With HMVEC there was no major interaction between the effect of albumin and chlorinated oleic acid on cell growth. In contrast, with IHKE albumin at low concentration abolished the growth inhibiting effect of chlorinated oleic acid and appreciably counteracted growth inhibition by the fatty acid of HepG2. We conclude that the growth modulation by chlorinated oleic acid and its interaction with vitamin E and albumin are cell specific.
