Effects of palm oil mill effluent media on cell growth and lipid content of Nannochloropsis oculata and Tetraselmis suecica

In this study, palm oil mill effluent (POME) was used as an alternative medium for algal biomass and lipid production. The influence of different concentrations of filtered and centrifuged POME in sea water (1, 5, 10 and 15%) on microalgal cell growth and lipid yield were investigated. Both Nannochloropsis oculata and Tetraselmis suecica had enhanced cell growth and lipid accumulation at 10% POME with maximum specific growth rate (0.21 d^–1 and 0.20 d^–1) and lipid content (39.1 ± 0.73% and 27.0 ± 0.61%), respectively, after 16 days of flask cultivation. The total Saturated Fatty Acid (SFA) (59.24%, 68.74%); Monounsaturated Fatty Acid (MUFA) (15.14%, 12.26%); and Polyunsaturated Fatty Acid (PUFA) (9.07%, 8.88%) were obtained for N. oculata and T. suecica, respectively, at 10% POME. Algal cultivation with POME media also enhanced the removal of Chemical Oxygen Demand (COD) (93.6–95%), Biological Oxygen Demand (BOD) (96–97%), Total Organic Compound (TOC) (71–75%), Total Nitrogen (TN) (78.8–90.8%) and oil and grease (92–94.9%) from POME.     

Biomarker responses as indication of contaminant effects in Oreochromis niloticus

The current study investigated oxidative stress parameters (enzymes activities, metallothionein content and lipid peroxidation) in freshwater fish, Oreochromis niloticus, tilapia exposure to Monjolinho River (in 4 months of year: January, April, July and November). One critical site in Monjolinho River (site B) was assessed in comparison to a reference site (site A). Water pH and oxygen concentration was lower than that recommended by CONAMA (Brazilian National Environmental Committee), resolution 357/2005 for protection of aquatic communities, and ammonium and the metals Cu, Zn, Mn and Fe (on all months) concentrations were higher than the maximum concentration recommended. Glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were significantly decreased in liver and muscle in tilapia from Monjolinho River, throughout the year, in relation to reference except in gills that SOD activity increased. Glutathione S-transferase (GST) activity was significantly increased in liver of the tilapia from Monjolinho River in all sites, in relation to reference except in gills that GST activity increased in July and decreased in November, suggesting that GST activity could be induced to neutralize the pollutants toxicity. On the other hand, GST activity was significantly decreased in white muscle indicating a toxic effect of pollutants, resulting in a decreased ability of tilapia to perform defense reactions associated to GSTs. The decrease of catalase (CAT) activity in gills of the O. niloticus together with the increase of SOD activity, could explain the increased lipid peroxidation (LPO) level in this organ. Metallothionein levels in liver and gills were significantly high in all sites. Results indicate that the exposure to metals caused severe damage to tissues; despite the consensually assumed antioxidant induction as a sign of exposure to contaminants the effects seem in part to be mediated by suppression of antioxidant system with SOD, CAT and GPx as potential candidates for tissues toxicity biomarkers of pollutants.     

Oxidative damage in gill of Mytilus edulis from Merseyside, UK, and reversibility after depuration

Mussels were collected from the urban/industrialized site of New Brighton, Merseyside and the relatively non-industrial site of Llandudno, North Wales. All mussels were identified as Mytilus edulis by PCR amplification of Mefp1. DNA single strand breaks and 8-oxo-7,8-dihydro-2'-deoxyguanosine were measured in gill within 24h of collection, using the COMET assay, both with and without formamidopyrimidine glycosylase. Gill lipid peroxidation was also measured within 24h. No difference between sites was found for frank SSB and malonaldehyde levels, however 8-oxo-dG and 4-hydroxynonenal were significantly greater in New Brighton mussels compared to Llandudno mussels. After 1-month laboratory maintenance, lipid peroxidation and 8-oxo-dG levels were lower. In contrast, frank SSB were higher. This could reflect enhanced DNA repair excision, though we cannot exclude the possibility of other non-oxidative DNA damage. The results suggest that laboratory maintenance allows recovery from environmentally induced oxidative damage, which was more extensive at Merseyside.     

Effects of lipid concentration on anaerobic co-digestion of municipal biomass wastes

The influence of the lipid concentration on the anaerobic co-digestion of municipal biomass waste and waste-activated sludge was assessed by biochemical methane potential (BMP) tests and by bench-scale tests in a mesophilic semi-continuous stirred tank reactor. The effect of increasing the volatile solid (VS) concentration of lipid from 0% to 75% was investigated. BMP tests showed that lipids in municipal biomass waste could enhance the methane production. The results of bench-scale tests showed that a lipids concentration of 65% of total VS was the inhibition concentration. Methane yields increased with increasing lipid concentration when lipid concentrations were below 60%, but when lipid concentration was set as 65% or higher, methane yields decreased sharply. When lipid concentrations were below 60%, the pH values were in the optimum range for the growth of methanogenic bacteria and the ratios of volatile fatty acid (VFA)/alkalinity were in the range of 0.2–0.6. When lipid concentrations exceeded 65%, the pH values were below 5.2, the reactor was acidized and the values of VFA/alkalinity rose to 2.0. The amount of Brevibacterium decreased with increasing lipid content. Long chain fatty acids stacked on the methanogenic bacteria and blocked the mass transfer process, thereby inhibiting anaerobic digestion.     

Lung subcellular fractions and surfactant lipid metabolism of rats exposed with DDT or endosulfan intratracheally

Abstract

The effect of intracheally administered DDT (5 mg/100 g body weight) or endosulfan (1 mg/100 g body weight) for three cosecutive days have been studied on lipid metabolism of rat lung subcellular fractions. Both the insecticides did not affect the lung weight and the protein contents of microsomes, lamellar bodies and surfactant but significantly increased the phospholipid contents of microsomal and surfactant system. Most of the neutral lipid components of lung subcellular fractions were also increased by DDT or endosulfan treatments, except that of surfactant triglycerides which were decreased by DDT treatment. DDT or endosulfan both increased the incorporation of radioactive [methyl‐³H]choline into microsomal phosphatidylcholine (PC) and surfactant dipalmitoylphosphatidylcholine (DPPC) without affecting the incorporation of radioactive [methyl‐¹⁴C]methionine, showing the increased synthesis of PC via CDPcholine pathway. The results presented in this communication showed that DDT and endosulfan, the two different chloroinsecticides have similar effects on microsomal lipid metabolism but produce different biochemical manifestations on the secretion of surfactant phospholipids.     

Changes in lipid profiles of liver microsomes of rats following intratracheal administration of DDT or endosulfan

Abstract

The effect of intratracheal administration of DDT (5 mg/100 g body weight) or endosulfan (1 mg/100 g body weight) to rats for three consecutive days, has been studied on liver lipid metabolism. The administration of DDT but not endosulfan significantly increased the liver weight and the microsomal protein contents. Both DDT and endosulfan treatments significantly increased the contents of microsomal phosphatidylcholine (PC), total‐free‐ and esterified cholesterol. The distribution of unsaturated fatty acids of microsomal PC and PE was increased by DDT treatment. The intratracheal administration of DDT caused fatty infiltration of liver which was probably due to increased synthesis of triglycerides (TG). This is supported by the increased incorporation of radioactive palmitate‐l‐¹⁴C into microsomal TG. However, the increased incorporation of palmitate‐l‐¹⁴C into microsomal PC and phosphatidylethanolamine (PE) after the DDT treatment, was due to the increased transacylation reaction supported by the decreased activity of microsomal phospholipase A. The intratracheal adminstration of endosulfan did not has pronounced effect on liver fatty infiltration, or transacylation reaction in microsomal PC and PE. However, the results have shown that the treatments of DDT or endosulfan increased the PC contents and the incorporation of radioactive [methyl‐³H]choline into PC of microsomes, resulting the increased synthesis of PC via CDPcholine pathway. Thus, the intratracheally administered DDT or endosulfan to rats showed that both the insecticides cause manifestations in the biochemistry of microsomal membrane lipids, although the effects of DDT being more pronounced. Therefore, the translocation effects of these insecticides or metabolites from lung to liver is established.     

Chemical self-organization in self-assembling biomimetic systems

Far-from-equillibrium oscillating chemical reactions are among the simplest systems showing complex behaviors and emergent properties. This class of reactions is often employed to mimic and understand the mechanisms of a great variety of biological processes. In this context, pattern formation due to the coupling between reaction and transport phenomena represent an active and promising research area. In this paper, we present results coming from experiments where we tried to blend the structural properties of self-assembled matrixes (sodium dodecyl sulphate micelles and phospholipid bilayers) together with the evolutive peculiarities of the Belousov–Zhabotinsky reaction. A series of interesting dynamical behaviors, like spatio-temporal chaos, stationary patterns and segmented waves, were found in reaction–diffusion and reaction–diffusion–convection experiments.     

LncRNA PU.1 AS regulates arsenic-induced lipid metabolism through EZH2/Sirt6/SREBP-1c pathway

Arsenic (As) is an omnipresent metalloid toxicant, which has elicited serious environmental pollution and health risky problems. Previous studies have uncovered that the As exposure could also cause markedly reduction of serum triglycerides in mice. However, the regulation mechanisms are still largely unknown. The present study is aimed to elucidate the molecular mechanisms of lncRNAs in As-induced lipid metabolic disequilibrium. We demonstrated that lncRNA PU.1 AS was significantly induced in the liver of As-feed mice companied with lower serum triglycerides contents; further in vitro experiment confirmed that PU.1 AS regulated liver cells lipid accumulation by nile red fluorescence staining. Intensive mechanistic investigations illustrated that PU.1 AS could interact with EZH2 protein to regulate its downstream target gene expression, and As-induced PU.1 AS attenuated EZH2-supppressed Sirt6 expression, thereafter leading to a decreased SREBP-1c protein expression, as well as the diminished synthesis of triglycerides in hepatocytes. In conclusion, this study provided a new lncRNA-related regulatory signaling pathway participating in As-induced abnormal lipid metabolism.     

A mixture of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and non-ortho polychlorinated biphenyls (PCBs) changed the lipid content of pregnant Long Evans rats

Pregnant Long Evans rats received 1.0 μg/kg of dioxin toxic equivalents (TEQ) by oral gavage on the 15th gestational day (GD 15), using a dosing mixture that contained two polychlorinated dioxins, four polychlorinated furans and three non-ortho polychlorinated biphenyls (PCBs). Rats were sacrificed on GD 16, GD 21 and postnatal day 4 (PND 4). The lipid content of fetus, pup, placenta and maternal liver, serum and adipose tissue were determined. Treated GD 16 and GD 21 fetuses had identical lipid content to the control group, yet the lipid content of treated pups on PND 4 was 32% higher than that of the control group. On the other hand, the lipid content of placenta, liver, and serum from the treated dams was 44–50%, 24%, and 38% lower than that of the control group, respectively. Thus, a low-dose mixture of dioxin-like compounds can cause changes in lipid content. The lipid content of offspring was not affected until they were exposed via lactation.     

Adverse effects of triclosan on kidney in mice: Implication of lipid metabolism disorders

Triclosan (TCS) is a ubiquitous antimicrobial used in daily consumer products. Previous reports have shown that TCS could induce hepatotoxicity, endocrine disruption, disturbance on immune function and impaired thyroid function. Kidney is critical in the elimination of toxins, while the effects of TCS on kidney have not yet been well-characterized. The aim of the present study was to investigate the effects of TCS exposure on kidney function and the possible underlying mechanisms in mice. Male C57BL/6 mice were orally exposed to TCS with the doses of 10 and 100 mg/(kg•day) for 13 weeks. TCS was dissolved in dimethyl sulfoxide (DMSO) and diluted by corn oil for exposure. Corn oil containing DMSO was used as vehicle control. Serum and kidney tissues were collected for study. Biomarkers associated with kidney function, oxidative stress, inflammation and fibrosis were assessed. Our results showed that TCS could cause renal injury as was revealed by increased levels of renal function markers including serum creatinine, urea nitrogen and uric acid, as well as increased oxidative stress, pro-inflammatory cytokines and fibrotic markers in a dose dependent manner, which were more significantly in 100 mg/(kg•day) group. Mass spectrometry-based analysis of metabolites related with lipid metabolism demonstrated the occurrence of lipid accumulation and defective fatty acid oxidation in 100 mg/(kg•day) TCS-exposed mouse kidney. These processes might lead to lipotoxicity and energy depletion, thus resulting in kidney fibrosis and functional decline. Taken together, the present study demonstrated that TCS could induce lipid accumulation and fatty acid metabolism disturbance in mouse kidney, which might contribute to renal function impairment. The present study further widens our insights into the adverse effects of TCS.