Plummeting toxic contaminates from water through phycoremediation: Mechanism, influencing factors and future outlook to enhance the capacity of living and non-living algae.

Freshwater habitats hold a unique role in the survival of all living organisms and supply water for drinking, irrigation, and life support activities. In recent decades, due to anthropogenic activities, deterioration in the water quality has been a long-lasting problem and challenge to the scientific fraternity. Although, these freshwater bodies have a bearable intrinsic capacity for pollution load however alarming increase in pollution limits the intrinsic capacities and requires additional technological interventions. The release of secondary pollutants from conventional interventions further needs revisiting the existing methodologies and asking for green interventions. Green interventions such as phycoremediation are natural, eco-friendly, economic, and energy-efficient alternatives and provide additional benefits such as nutrient recovery, biofuel production, and valuable secondary metabolites from polluted freshwater bodies. This systemic review in a nut-shell comprises the recent research insights on phycoremediation, technological implications, and influencing factors, and further discusses the associated mechanisms of metal ions biosorption by living and non-living algae, its advantages, and limitations. Besides, the article explores the possibility of future research prospects for applicability at a field scale that will help in the efficient utilization of resources, and improved ecological and health risks.

A novel dodecapeptide from a combinatorial synthetic library exhibits potent antifungal activity and synergy with standard antimycotic agents.

There has been a marked expansion in the discovery of new antifungal peptides. This paper describes a novel dodecapeptide, H-Arg-Trp-Trp-Arg-D-Trp-D-Phe-Ile-D-Phe-His-Trp-Arg-Trp-NH(2), derived from a previously described nonapeptide and synthesized by the combinatorial approach. Further, interaction of this peptide with antifungals such as amphotericin B, flucytosine and fluconazole was studied by checkerboard analysis and time-kill assay to obtain the dynamic picture with respect to time. The best synergistic activity was observed with a combination of peptide and fluconazole, followed by peptide and flucytosine.

Assessment of background gamma radiation levels using airborne gamma ray spectrometer data over uranium deposits, Cuddapah Basin, India - A comparative study of dose rates estimated by AGRS and PGRS.

The Atomic Minerals Directorate for Exploration and Research (AMD) has conducted high-resolution airborne gamma ray spectrometer (AGRS), magnetometer and time domain electromagnetic (TDEM) surveys for uranium exploration, along the northern margins of Cuddapah Basin. The survey area includes well known uranium deposits such as Lambapur-Peddagattu, Chitrial and Koppunuru. The AGRS data collected for uranium exploration is utilised for estimating the average absorbed rates in air due to radio-elemental (potassium in %, uranium and thorium in ppm) distribution over these known deposit areas. Further, portable gamma ray spectrometer (PGRS) was used to acquire data over two nearby locations one from Lambapur deposit, and the other from known anomalous zone and subsequently average gamma dose rates were estimated. Representative in-situ rock samples were also collected from these two areas and subjected to radio-elemental concentration analysis by gamma ray spectrometer (GRS) in the laboratory and then dose rates were estimated. Analyses of these three sets of results complement one another, thereby providing a comprehensive picture of the radiation environment over these deposits. The average absorbed area wise dose rate level is estimated to be 130 ± 47 nGy h-1 in Lambapur-Peddagattu, 186 ± 77 nGy h-1 in Chitrial and 63 ± 22 nGy h-1 in Koppunuru. The obtained average dose levels are found to be higher than the world average value of 54 nGy h-1. The gamma absorbed dose rates in nGy h-1 were converted to annual effective dose rates in mSv y-1 as proposed by the United Nations Scientific Committee on the Effect of Atomic Radiation (UNSCEAR). The annual average effective dose rates for the entire surveyed area is 0.12 mSv y-1, which is much lower than the recommended limit of 1 mSv y-1 by International Commission on Radiation protection (ICRP). It may be ascertained here that the present study establishes a reference data set (baseline) in these areas to assess any changes in gamma radiation levels due to mining and milling activities in future.

Correlation of various histopathologic prognostic factors with Nottingham prognostic index and microvessel density in invasive breast carcinoma: A study of 100 cases.

BACKGROUND: Nottingham prognostic index (NPI) is a widely used integrated prognostic variable in patients with breast cancer. NPI has been correlated with tumor size, grade, lymph node stage and patient survival. The present study aimed at evaluating and correlating the various clinical and pathologic features of breast carcinoma with NPI. METHODS: This study included 100 consecutive cases of primary breast carcinoma over a period of 2 years. Demographic data was noted and histomorphological features like tumor size, grade, lymph node involvement, necrosis, vascular invasion etc., were assessed. NPI was calculated as reported in the literature. Immunohistochemical staining for hormone receptors and CD34 (to calculate microvessel density [MVD]) was performed. Statistical analysis was used for correlation. RESULTS: Of the 100 cases, 54% of the tumors were in T2 tumor size category (2-5 cm) and lymph node metastasis in 48% of the cases. NPI ranged from 2.3 to 7.3 with 54% of the cases in the intermediate NPI group (3.41-5.4). The mean MVD was 160.93 (±69.4/mm2). On statistical analysis, tumor size and grade, lymph node stage, mitotic rate, nuclear pleomorphism, necrosis and MVD showed a correlation with NPI (P < 0.05). CONCLUSION: NPI is an important and useful prognostic indicator for breast cancer patients, which shows the correlation with other histomorphological prognostic features as well.

1(2-benzoylethyl)pyridinium chloride: a new potent and selective inhibitor of bovine brain and human placental choline acetyltransferase.

A newly synthesized 1(2-benzoylethyl)pyridinium (BEP), an analog of the choline acetyltransferase (ChA) inhibitor (2-benzoylethyl)trimethylammonium (BETA), was evaluated for its ability to inhibit ChA from bovine brain and human placenta. Its ChA inhibitory properties were compared with that of BETA. BEP was found to be an effective inhibitor of ChA (I50: 10-18 microM). BEP, as well as BETA, was a linear noncompetitive inhibitor of ChA with respect to both substrates, acetylcoenzyme A and choline. BEP and BETA were poor inhibitors of electric eel acetylcholinesterase. These observations indicate that BEP is a potent and selective inhibitor of ChA. Furthermore, because of the possible delocalization of the positive charge at the N atom of the BEP molecule throughout the pyridine ring, it is anticipated that BEP would have a higher potential for lipid solubility, stability and selectivity than BETA.

Influence of phencyclidine on the translocation of pentobarbital in mice.

The influence of phencyclidine (PCP) on the tissue distribution of pentobarbital in male Swiss mice (20-25 g) was investigated. Animals pretreated with PCP (179 mumol/kg/day) for 4 days, i.p., were administered pentobarbital (60 mg/kg, i.p.) 24 h after the PCP injection, sacrificed at various time intervals, and tissues (serum, brain, liver and kidney) were collected. Pentobarbital levels in tissues were determined by the gas liquid chromatography. When compared to the control group, PCP treatment decreased the pentobarbital level by 68% in liver and increased the level by 97% in kidney at 45 min post-injection. No significant change in serum and brain pentobarbital level was noted with either group. These data indicate that PCP influences the translocation of pentobarbital.

The role of hepatic microsomal enzymes in the modulation of phencyclidine-induced toxicity.

The LD50 of phencyclidine (PCP, 234 mumol/kg, i.p.) in male Swiss mice decreased by 62% in animals pretreated with 2-diethylamino-2,2-diphenylvalerate hydrochloride (SKF-525A, 40 mg/kg), and increased by 74% and 20% in animals pretreated with sodium phenobarbital (75 mg/kg), and 3-methylcholanthrene (70 mg/kg), respectively, No Significant change in the LD50 was observed with cysteine or diethylmaleate pretreatment. The treatment with PCP at 179 mumol/kg/day i.p. for 7 days resulted in body weight decrement in the first 2 days and gradual increment thereafter. The increase was only 33% of the control group. The food intake was also lower in the PCP treated group of animals. PCP withdrawal led to an increase in food intake as well as body weight at a normal rate. The ratio of liver weight to body weight was not significantly higher than that of control during the treatment period. The administration of PCP for 7 days did not alter the activities of liver function enzyme markers. However, within 12 h of the initial PCP treatment a 85% increase in activity of serum glutamicoxalacetic transaminase was observed. Later the enzyme activity reached close to normal levels. No liver lesions at the light microscopic level were observed. Treatment of mice for 4 days with PCP (179 mumol/kg) caused no significant change in pentobarbital sleeping time.

Substituted thiazolidones: selective inhibition of nicotinamide adenine dinucleotide-dependent oxidations and evaluation of their CNS activity.

Eight 2-arylimino-3-(3-N-morpholinopropyl) thiazolid-4-ones were synthesized from the corresponding 1-aryl-3-(3-N-morpholinopropyl) thiocarbamides, characterized, and tested for their effects on the cellular respiratory activity of rat brain homogenates. All substituted 4-thiazolidones selectively inhibited nicotinamide adenine dinucleotide (NAD)-dependent oxidations of pyruvate, citrate, DL-isocitrate, alpha-ketoglutarate, malate, beta-hydroxybutyrate, L-glutamate, and NADH, while the NAD-independent oxidation of succinate remained unaltered. All thiazolidones possessed some degree of anticonvulsant activity against pentylenetetrazol-induced convulsions, and the protection afforded by these compounds at a dose of 100 mg/kg ranged from 30 to 80%. The low toxicity possessed by most of these thiazolidones was reflected by their approximate LD-50 values from 300 mg/kg to greater than 1000 mg/kg. In the present study, the anticonvulsant activity possessed by these substituted 4-thiazolidones was unrelated to their ability to inhibit selectively the NAD-dependent oxidations by rat brain homogenates. These thiazolidones exhibited depression of the CNS activity which, in some cases, was associated with the increase in respiration. All thiazolidones potentiated pentobarbital (sodium) sleeping time in mice when administered in a dose of 100 mg/kg.

Synthesis of N,N'-bis(3-substituted benzylideneaminopropyl)-piperazines and their anti-inflammatory, antiproteolytic, and anticonvulsant properties.

Some N,N'-bis(3-substituted benzylideneaminopropyl) piperazines were synthesized and characterized by their sharp melting points and elemental analyses. These substituted piperazines possessed anti-inflammatory activity, and the protection afforded by these compounds against carrageenan-induced edema ranged from 23 to 67%. The antiproteolytic activity of these piperazines was reflected by their ability to inhibit in vitro hydrolysis of bovine serum albumin and casein by trypsin. The inhibition of trypsin-induced hydrolysis was concentration dependent and competitive in nature.

Relationships between chemical structure and inhibition of human placental choline acetyltransferase by keto analogs of acetylcholine.

Seven keto analogs of acetylcholine were synthesized and evaluated as inhibitors of human placental choline placental choline acetyltransferase. Their potencies for inhibition of horse serum cholinesterase and stimulation of cholinergic receptors in the longitudinal ileal muscle of the guinea pig were investigated. The most potent and selective inhibitor of choline acetyltransferase was (2-benzoylethyl)trimethylammonium chloride with an I50 of 3 X 10(-6) M. It exhibited considerably low activities at muscarinic and nicotinic receptors and cholinesterases. Its high potency for inhibiting choline acetyltransferase was atrributed to: (a) its cationic terminal, a site for an electron acceptor interaction; (b) an aryl moiety for hydrophobic and electron donor contributions; and (c) a positive charge on the carbon atom adjacent to the benzene ring due to the presence of the carbonyl group, which interacts with the nucleophilic residue on the enzyme.

Anticonvulsant activity of N,N'-bis[3-(3-substituted urea)propyl]piperazines.

Several N,N'-bis[3-(3-substituted urea)propyl]piperazines were synthesized and characterized by their sharp melting points, elemental analyses, and IR spectra. All substituted piperazines were found to possess anticonvulsant activity, which was reflected by 20-70% protection observed against pentylenetetrazol-induced seizures in mice. Some of these compounds inhibited oxidation of pyruvic acid by rat brain homogenate. No correlation could be observed between the anticonvulsant activity possessed by these substituted piperazines and their ability to inhibit the oxidation of pyruvic acid.

CNS depressant activity of pyrimidylthiazolidones and their selective inhibition of NAD-dependent pyruvate oxidation.

Several 1-aryl-3-(2-pyrimidyl)thiocarbamides and their corresponding cyclized 2-arylimino-3-(2-pyrimidyl)thiazolid-4-ones were synthesized and characterized by their sharp melting points and elemental analyses. These thiocarbamides and thiazolidones possessed anticonvulsant activity against pentylenetetrazol-induced convulsions and potentiated pentobarbital-induced hypnosis in mice. Most of these thiocarbamides and thiazolidones selectively inhibited nicotinamide adenine dinucleotide (NAD)-dependent oxidation of pyruvate, where the use of added NAD dether hand, remained unaltered. The anticonvulsant activity of thiocarbamides and thiazolidones was unrelated to their ability to inhibit the respiratory activity of rat brain homogenates during oxidation of sodium pyruvate. Cyclization of thiocarbamides to the corresponding thiazolidones in general enhanced their CNS depressant and enzyme inhibitory effectiveness.

Effects of mecamylamine, nicotine, atropine and physostigmine on the phencyclidine-induced behavioral toxicity.

Phencyclidine (PCP) has multifaceted actions on the cholinergic functions, including interaction with the central and peripheral cholinergic receptors. Therefore, to evaluate the possible involvement of the nicotinic and muscarinic acetylcholine (ACh) receptors during the behavioral toxicity of PCP, influence of various cholinergic modifiers on the PCP-induced behavioral effects in male Swiss mice was studied. PCP-induced (45 mumol/kg, IP) behavioral toxicity (circular movements, side-to-side head movements, and hyperactivity leading to convulsions) was blocked by pretreating the animals with secondary- or tertiaryamino -cholinergic modifiers, mecamylamine (ME; 14.9 and 29.9 mumol/kg), nicotine (NI; 12.3 and 30.8 mumol/kg) and physostigmine (PH; 0.16 and 0.31 mumol/kg). NI at 1.5 mumol/kg significantly potentiated the PCP-induced convulsions. Atropine (AT; 14.4 and 28.8 mumol/kg) pretreatments shortened the onset of circular movements. The locomotor activity of PCP (16.4 mumol/kg) was blocked by ME, NI, and PH. AT at 7.2 mumol/kg significantly potentiated the PCP-locomotion by 62%. These observations indicated that the behavioral actions of PCP, at least in part, are mediated by the central nicotinic and muscarinic ACh receptors. The involvement of cholinergic receptors in conjunction with the dopaminergic actions of PCP during these behaviors also has been discussed.

Interaction between phencyclidine and its pyrolysis product, 1-phenylcyclohexene.

The interaction between phencyclidine (PCP) and its pyrolysis product, 1-phenylcyclohexene (PC), at metabolic level was evaluated in Swiss male mice (21-24 g). PC (1.1, 2.2 and 4.4 mmol/kg/day for 4 days, IP, in corn oil) treatment to mice induced the in vitro metabolism (p less than 0.05) of amidopyrine (17%), aniline (12%), phenacetin (62-100%), pentobarbital (20-26%), PCP (25-80%) and benzo[a]pyrene (81-147%) in the 9000 g liver fraction and the hepatic microsomal contents of cytochrome P-450 (18-42%). The induction of the mixed function oxygenase (MFO) system was consistent with the decreases in the concentrations of IP administered pentobarbital (0.27 mmol/kg, in saline) and PCP (16.4, 32.8 and 65.6 mumol/kg, in saline) in the serum, brain, liver and kidneys of PC pretreated mice. At 1 hr after the above doses of PC, the in vitro metabolism of amidopyrine, aniline, or phenacetin was not inhibited. However, the biotransformation of benzo[a]pyrene was inhibited by 33 to 45%. Though PC after a single dose did not alter the tissue concentrations of PCP, it increased the pentobarbital concentrations in the tissues studied (p less than 0.05). These results indicate that PC has a potential to induce the MFO system after the 4-day treatment. This property of PC plays an important role in the reduction of the action of PCP by enhancing its metabolism, thereby decreasing its tissue levels.

Toxicological findings in a multi-drug death involving propoxyphene, caffeine, phenacetin, acetaminophen and salicylate.

The toxicological findings of a multi-drug related fatal poisoning are described here. A 35-year-old Caucasian male found dead on the kitchen floor was a known user of abused drugs and had been taking aspirin alone or in combination with phenacetin and caffeine for the relief of joint pains. The gross examination of the organs at autopsy revealed slight grooving of the uncus and various stages of necrosis in the renal papillae. Histological examination confirmed the gross appearance of pulmonary congestion and edema, cerebral edema and interstitial nephritis of the tubules. Toxicological evaluation of the blood and urine samples disclosed the presence of propoxyphene (51 and 250 mg/l), salicylate (185 and 2750 mg/l), caffeine (16 and 37 mg/l), and phenacetin (9.6 and 20 mg/l). Furthermore, acetaminophen also was present in the plasma (54 mg/l) and urine. A gas liquid chromatographic method for simultaneous analysis of phenacetin and caffeine utilizing a nitrogen phosphorus detector was proposed.

A multi-chemical death involving caffeine, nicotine and malathion.

Death of a 21-year-old man who was found in a shower stall in his residence is described in the study. At the scene, a 3/4 filled blue glass bottle labeled "Black Leaf 40" (an insecticide containing nicotine), a white plastic pitcher 1/3 full of thick white fluid, a beer mug 1/4 full of thick white fluid, and an empty carton of milk were found. In addition, a can of malathion and an empty bottle labeled caffeine also were found in the vicinity. Autopsy was performed, and the gross examinations of organs revealed no specific findings to account for the death. However, marked congestion in lung, liver, spleen and kidney were noted at microscopic level. Autolytic degenerative changes were also observed in stomach, small bowel and colon. Toxicological analyses of the autopsy samples (blood, urine, liver and gastric contents) revealed the presence of caffeine and nicotine in each sample. Malathion was found to be present only in gastric content. Caffeine and nicotine were analyzed by utilizing gas liquid chromatography-nitrogen phosphorus detector, while malathion was by gas liquid chromatography-flame photometric detector. Analyses of the fluids from the bottle, pitcher and mug disclosed the presence of nicotine in the concentrations of 17.8%, 3.7% and 5.7% (w/w), respectively. The fluids from the pitcher and mug also contained 2.7-2.9% malathion. Results conclude the death was associated with caffeine, nicotine and malathion.

Genotyping for DQA1 and PM loci in urine using PCR-based amplification: effects of sample volume, storage temperature, preservatives, and aging on DNA extraction and typing.

Urine is often the sample of choice for drug screening in aviation/general forensic toxicology and in workplace drug testing. In some instances, the origin of the submitted samples may be challenged because of the medicolegal and socioeconomic consequences of a positive drug test. Methods for individualization of biological samples have reached a new boundary with the application of the polymerase chain reaction (PCR) in DNA profiling, but a successful characterization of the urine specimens depends on the quantity and quality of DNA present in the samples. Therefore, the present study investigated the influence of storage conditions, sample volume, concentration modes, extraction procedures, and chemical preservations on the quantity of DNA recovered, as well as the success rate of PCR-based genotyping for DQA1 and PM loci in urine. Urine specimens from male and female volunteers were divided and stored at various temperatures for up to 30 days. The results suggested that sample purification by dialfiltration, using 3000-100,000 molecular weight cut-off filters, did not enhance DNA recovery and typing rate as compared with simple centrifugation procedures. Extraction of urinary DNA by the organic method and by the resin method gave comparable typing results. Larger sample volume yielded a higher amount of DNA, but the typing rates were not affected for sample volumes between 1 and 5 ml. The quantifiable amounts of DNA present were found to be greater in female (14-200 ng/ml) than in male (4-60 ng/ml) samples and decreased with the elapsed time under both room temperature (RT) and frozen storage. Typing of the male samples also demonstrated that RT storage samples produced significantly higher success rates than that of frozen samples, while there was only marginal difference in the DNA typing rates among the conditions tested using female samples. Successful assignment of DQA1 + PM genotype was achieved for all samples of fresh urine, independent of gender, starting sample volume, or concentration method. Preservation by 0.25% sodium azide was acceptable for sample storage at 4 degrees C during a period of 30 days. For longer storage duration, freezing at -70 degrees C may be more appropriate. Thus, the applicability of the DQA1 + PM typing was clearly demonstrated for individualization of urine samples.

Blood carbon monoxide and hydrogen cyanide concentrations in the fatalities of fire and non-fire associated civil aviation accidents, 1991-1998.

Blood samples submitted to the Civil Aeromedical Institute (CAMI) from aviation accident fatalities are analyzed for carbon monoxide (CO), as carboxyhemoglobin (COHb), and hydrogen cyanide, as cyanide (CN(-)). These analyses are performed to establish possible exposure of victims to smoke from in-flight/post-crash fires or to CO from faulty exhaust/heating systems. The presence of both gases in blood would suggest that the victim was alive and inhaled smoke. If only COHb is elevated, the accident (or a death) could be the result of CO contamination of the interior. Information pertaining to blood levels of these gases in aviation fatalities, in relation to the associated accidents, is scattered or not available, particularly with regard to toxicity. Therefore, considering that COHb> or =10% and CN(-)> or =0.25 microg/ml are sufficient to produce some degree of toxicological effects, the necessary information was extracted from the CAMI database. Samples from 3857 fatalities of 2837 aviation accidents, occurring during 1991-1998, were received; 1012 accidents, encompassing 1571 (41%) fatalities, were fire associated, whereas 1820 accidents were non-fire related. The remaining five accidents were of unknown fire status. There were fewer fire related fatalities and associated accidents in the (COHb> or =10% and CN(-)> or =0.25 microg/ml) category than that in the (COHb<10% and CN(-)<0.25 microg/ml) category. No in-flight fire was documented in the former category, but in-flight fires were reported in 14 accidents (18 fatalities) in the latter category. No non-fire accident fatality was found wherein levels of both gases were determined to be at or above the stated levels. There were 15 non-fire accidents with 17 fatalities wherein only COHb (10-69%) was elevated. The present study suggests that aviation fire accidents/fatalities were fewer than aviation non-fire accidents/fatalities and confirms that aviation accidents related to in-flight fires and CO-contaminated interiors are rare.

A fatality caused by accidental production of hydrogen sulfide.

A 55-year-old male Caucasian truck driver was dead at the scene after breathing hydrogen sulfide (H(2)S) produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H(2)SO(4)) and iron(II) sulfate (FeSO(4)). Autopsy of the decedent's body revealed pulmonary edema and passive congestion in lungs, spleen, kidneys, and adrenal glands. Postmortem biological samples were analyzed for carbon monoxide, cyanide, ethanol, and drugs. Since a potential exposure to H(2)S was involved, blood was also analyzed for sulfide (S(2-)). The analysis entailed isolating S(2-) from blood as H(2)S using 0.5M H(3)PO(4), trapping the gas in 0.1M NaOH, and determining the electromotive force using a sulfide ion specific electrode. Acetaminophen at a concentration of 14.3 microg/ml was found in blood, and metoprolol was detected in the blood, liver, and kidney samples. The blood S(2-) level was determined to be 1.68 microg/ml. It is concluded that the cause of death was H(2)S poisoning associated with a hazardous material accident in an industrial situation.

Two tricyclic antidepressant poisonings: levels of amitriptyline, nortriptyline and desipramine in post-mortem biological samples.

Two deaths due to amitriptyline and desipramine overdoses are reported. The first case deals with a 20-year-old Caucasian male who was found dead at his residence. Toxicological analysis of the blood, urine, liver and kidney revealed the presence of amitriptyline (1.7 mg/l, 0.13 mg/l, 36.0 mg/kg and 98.0 mg/kg) and nortriptyline (0.66 mg/l, 0.74 mg/l, 12.0 mg/kg and 37.0 mg/kg). The gastric content contained only 220 mg of amitriptyline. The urine also contained norverapamil, which was consistent with previous verapamil therapy. The second case involved a 19-year-old Caucasian male who attempted suicide earlier and was on desipramine medication. The blood, urine, liver and gastric content disclosed the presence of desipramine in the concentrations of 14.2 mg/l, 33.7 mg/l, 112.5 mg/kg and 180 mg, respectively. The levels of these tricyclics analyzed by high pressure liquid chromatography were in agreement with the levels reported in the literature. Though with the amitriptyline poisoning no significant anatomic changes were noted, the desipramine-caused death was further supported by the multisystem vascular congestion and ischemic changes consistent with cardiopulmonary failure.