Revealing on hydrogen sulfide and nitric oxide signals co-ordination for plant growth under stress conditions.

In the recent times, plants are facing certain types of environmental stresses, which give rise to formation of reactive oxygen species (ROS) such as hydroxyl radicals, hydrogen peroxides, superoxide anions and so on. These are required by the plants at low concentrations for signal transduction and at high concentrations, they repress plant root growth. Apart from the ROS activities, hydrogen sulfide (H2 S) and nitric oxide (NO) have major contributions in regulating growth and developmental processes in plants, as they also play key roles as signaling molecules and act as chief plant immune defense mechanisms against various biotic as well as abiotic stresses. H2 S and NO are the two pivotal gaseous messengers involved in growth, germination and improved tolerance in plants under stressed and non-stress conditions. H2 S and NO mediate cell signaling in plants as a response to several abiotic stresses like temperature, heavy metal exposure, water and salinity. They alter gene expression levels to induce the synthesis of antioxidant enzymes, osmolytes and also trigger their interactions with each other. However, research has been limited to only cross adaptations and signal transductions. Understanding the change and mechanism of H2 S and NO mediated cell signaling will broaden our knowledge on the various biochemical changes that occur in plant cells related to different stresses. A clear understanding of these molecules in various environmental stresses would help to confer biotechnological applications to protect plants against abiotic stresses and to improve crop productivity.

A Systematic Review of Radiological Diagnosis and Management of May-Thurner Syndrome.

May-Thurner syndrome (MTS) is an anatomical condition of external luminal compression of common iliac vein due to a partial obstruction of the common iliac vein between common iliac artery and lumbar vertebra causes deep-vein thrombosis, venous hypertension, and chronic venous insufficiencies. In this article, we review present evidence of the clinical diagnosis and management of MTS. Here, we conducted a literature review of studies on MTS. We also reviewed different clinical features, presentation, diagnostic methods, and therapeutic procedure for this condition. Most studies mentioned the diagnosis of this condition is performed by color Doppler, computed tomographic angiography, venography, and problem-solving cases by intravascular ultrasound technique. Nonsurgical methods of management are first line, and vascular surgery is reserved for refractory cases. Multiple modalities are required to reach the diagnosis of MTS, and noninvasive intervention radiology methods are the first line of management. This review highlights the presentations of MTS and outlines diagnostic procedure and management.

A critical review of concentrating and nanofluid-based hybrid PV/T systems utilizing beam splitting technique: Progress, challenges, and way forward.

The utilization of nanofluids and concentrating techniques in solar photovoltaic/thermal (PV/T) systems, to enhance the overall system performance, have been analysed explicitly in the last few years. More recently, nanofluid-based optical filters were integrated with photovoltaic (PV) systems for the effective utilization of solar spectrum, i.e. below and beyond the band-gap of PV cells. Therefore, to quantify the recent progress of spectral beam splitting-based hybrid PV/T systems (BSPV/T), a systematic review has been presented therein. The study highlights the technological and scientific advancement in BSPV/T in last two decades. Linear Fresnel mirror-based BSPV/T showed significant enhancement in the overall performance of hybrid PV/T system. Recently developed nanoparticle-laden BSPV/T system shows significant improvement in overall thermal efficiency of BSPV/T system, thanks to decoupling of thermal system and PV cell. Further, economic analysis, carbon footprint, and environmental assessment of BSPV/T are also discussed briefly. At the last, the authors have made an effort to identify the challenges, limitations, and prospective paths for future research in BSPV/T systems.

Influence of CYP2C9, GSTM1, GSTT1 and NAT2 genetic polymorphisms on DNA damage in workers occupationally exposed to organophosphate pesticides.

Previous studies have revealed that organophosphate pesticides (OPs) are primarily metabolized by xenobiotic metabolizing enzymes (XMEs). Very few studies have explored genetic polymorphisms of XMEs and their association with DNA damage in pesticides-exposed workers. Present study was designed to determine the influence of CYP2C9, GSTM1, GSTT1 and NAT2 genetic polymorphisms on DNA damage in workers occupationally exposed to OPs. We examined 268 subjects including 134 workers occupationally exposed to OPs and an equal number of normal healthy controls. The DNA damage was evaluated using alkaline comet assay and genotyping was done using individual polymerase chain reaction (PCR) or polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Acetylcholinesterase and paraoxonase activity were found to be significantly lowered in workers as compared to control subjects which were analyzed as biomarkers of toxicity due to OPs exposure (p<0.001). Workers showed significantly higher DNA tail moment (TM) compared to control subjects (14.32±2.17 vs. 6.24±1.37 tail % DNA, p<0.001). GSTM1 null genotype was found to influence DNA TM in workers (p<0.05). DNA TM was also found to be increased with concomitant presence of NAT2 slow acetylation and CYP2C9*3/*3 or GSTM1 null genotypes (p<0.05). DNA TM was found increased in NAT2 slow acetylators with mild and heavy smoking habits in control subjects and workers, respectively (p<0.05). The results of this study suggest that GSTM1 null genotypes, and an association of NAT2 slow acetylation genotypes with CYP2C9*3/*3 or GSTM1 null genotypes may modulate DNA damage in workers occupationally exposed to OPs.

Paraoxonase-1 genetic polymorphisms and susceptibility to DNA damage in workers occupationally exposed to organophosphate pesticides.

Human paraoxonase 1 (PON1) is a lipoprotein-associated enzyme involved in the detoxification of organophosphate pesticides (OPs) by hydrolyzing the bioactive oxons. Polymorphisms of the PON1 gene are responsible for variation in the expression and catalytic activity of PON1 enzyme. In the present study, we have determined (a) the prevalence of two common PON1 polymorphisms, (b) the activity of PON1 and acetylcholinesterase enzymes, and (c) the influence of PON1 genotypes and phenotypes variation on DNA damage in workers exposed to OPs. We examined 230 subjects including 115 workers exposed to OPs and an equal number of normal healthy controls. The results revealed that PON1 activity toward paraoxon (179.19±39.36 vs. 241.52±42.32nmol/min/ml in controls) and phenylacetate (112.74±17.37 vs. 134.28±25.49µmol/min/ml in controls) was significantly lower in workers than in control subjects (p<0.001). No significant difference was observed in the distribution of genotypes and allelic frequencies of PON1(192)QR (Gln/Arg) and PON1(55)LM (Leu/Met) in workers and control subjects (p>0.05). The PON1 activity toward paraoxonase was found to be significantly higher in the R/R (Arg/Arg) genotypes than Q/R (Gln/Arg) and lowest in Q/Q (Gln/Gln) genotypes in both workers and control subjects (p<0.001). For PON1(55)LM (Leu/Met), PON1 activity toward paraoxonase was observed to be higher in individuals with L/L (Leu/Leu) genotypes and lowest in individuals with M/M (Met/Met) genotypes in both groups (p<0.001). No influence of PON1 genotypes and phenotypes was seen on the activity of acetylcholinesterase and arylesterase. The DNA damage was observed to be significantly higher in workers than in control subjects (p<0.05). Further, the individuals who showed least paraoxonase activity i.e., those with (Q/Q [Gln/Gln] and M/M [Met/Met]) genotypes showed significantly higher DNA damage compared to other isoforms in workers exposed to OPs (p<0.05). The results indicate that the individuals with PON1 Q/Q and M/M genotypes are more susceptible toward genotoxicity. In conclusion, the study suggests wide variation in enzyme activities and DNA damage due to polymorphisms in PON1 gene, which might have an important role in the identification of individual risk factors in workers occupationally exposed to OPs.

Role of genetic polymorphisms of CYP1A1, CYP3A5, CYP2C9, CYP2D6, and PON1 in the modulation of DNA damage in workers occupationally exposed to organophosphate pesticides.

Organophosphate pesticides (OPs) are primarily metabolized by several xenobiotic metabolizing enzymes (XMEs). Very few studies have explored genetic polymorphisms of XMEs and their association with DNA damage in pesticide-exposed workers. The present study was designed to determine the role of genetic polymorphisms of CYP1A1, CYP3A5, CYP2C9, CYP2D6, and PON1 in the modulation of DNA damage in workers occupationally exposed to OPs. We examined 284 subjects including 150 workers occupationally exposed to OPs and 134 normal healthy controls. The DNA damage was evaluated using the alkaline comet assay and genotyping was done using PCR-RFLP. The results revealed that the PONase activity toward paraoxonase and AChE activity was found significantly lowered in workers as compared to control subjects (p<0.001). Workers showed significantly higher DNA damage compared to control subjects (14.37±2.15 vs. 6.24±1.37 tail% DNA, p<0.001). Further, the workers with CYP2D6*3PM and PON1 (QQ and MM) genotypes were found to have significantly higher DNA damage when compared to other genotypes (p<0.05). In addition, significant increase in DNA damage was also observed in workers with concomitant presence of certain CYP2D6 and PON1 (Q192R and L55M) genotypes which need further extensive studies. In conclusion, the results indicate that the PON1 and CYP2D6 genotypes can modulate DNA damage elicited by some OPs possibly through gene-environment interactions.

Genetic polymorphisms of GSTM1, GSTT1 and GSTP1 and susceptibility to DNA damage in workers occupationally exposed to organophosphate pesticides.

GSTM1, T1 and P1 are important enzymes of glutathione S-transferases (GSTs), involved in the metabolism of many endogenous and exogenous compounds. Individual genetic variation in these metabolizing enzymes may influence the metabolism of their substrates. The present study was designed to determine the genotoxic effects using DNA damage and its association with GSTM1, GSTT1, and GSTP1 (Ile105Val) genetic polymorphisms in workers occupationally exposed to organophosphate pesticides (OPs). We examined 230 subjects including 115 workers occupationally exposed to OPs and an equal number of normal healthy controls. The DNA damage was evaluated using the alkaline comet assay and genotyping was done using individual PCR or PCR-RFLP. Significantly higher DNA tail moment (TM) was observed in workers as compared to control subjects (14.41 ± 2.25 vs. 6.36 ± 1.41 tail % DNA, p<0.001). The results revealed significantly higher DNA TM in workers with GSTM1 null genotype than those with GSTM1 positive (15.18 vs. 14.15 tail % DNA, p=0.03). A significantly higher DNA TM was also observed in workers with homozygous Ile-Ile GSTP1 genotype than heterozygous (Ile-Val) and mutant (Val-Val) GSTP1 genotype (p=0.02). In conclusion, the results show that null deletion of GSTM1 and homozygote wild GSTP1 genotype could be related to inter-individual differences in DNA damage arises from the gene-environment interactions in workers occupationally exposed to OPs.

Physiological responses, tolerance, and remediation strategies in plants exposed to metalloids.

Metalloids are a subset of particular concern to risk assessors and toxicologists because of their well-documented potential hazards to plant system. Most of the metalloids are major environmental contaminants which affect crop productivity when present in high concentrations in soil. Metalloids are coupled with carrier proteins of the plasma membrane and translocated to various organs causing changes in key metabolic processes, damages cell biomolecules, and finally inhibit its growth. Phytoremediation-based approaches help in understanding the molecular and biochemical mechanisms for prerequisite recombinant genetic approaches. Recent advancements in proteomics and plant genomics help in understanding the role of transcription factors, metabolites, and genes in plant system which confers metal tolerance. The present review summarizes our current status of knowledge in this direction related to various physiological responses, detoxification mechanisms, and remediation strategies of metalloids in crop plants in relation to plant-metalloid tolerance. Further, the role of various transcription factors and miRNAs in conferring metal tolerance is also briefed. Hence, the present review mainly focused on the alterations in the physiological activities of plants due to metalloid toxicity and the various mechanisms which get activated inside the plants to mitigate their toxic effects.

Herbicide Glyphosate: Toxicity and Microbial Degradation.

Glyphosate is a non-specific organophosphate pesticide, which finds widespread application in shielding crops against the weeds. Its high solubility in hydrophilic solvents, especially water and high mobility allows the rapid leaching of the glyphosate into the soil leading to contamination of groundwater and accumulation into the plant tissues, therefore intricating the elimination of the herbicides. Despite the widespread application, only a few percentages of the total applied glyphosate serve the actual purpose, dispensing the rest in the environment, thus resulting in reduced crop yields, low quality agricultural products, deteriorating soil fertility, contributing to water pollution, and consequently threatening human and animal life. This review gives an insight into the toxicological effects of the herbicide glyphosate and current approaches to track and identify trace amounts of this agrochemical along with its biodegradability and possible remediating strategies. Efforts have also been made to summarize the biodegradation mechanisms and catabolic enzymes involved in glyphosate metabolism.

Genetic polymorphism of glutathione S-transferase M1 and T1 in Delhi population of Northern India.

Glutathione S-transferases (GSTs), protect cells from reactive chemical intermediates and oxidative stress. Among different classes of GSTs, GSTM1 (Mu) and GSTT1 (theta) are found to be genetically deleted. Present study was intended to genotype homozygous null distribution of GSTM1 and GSTT1 in healthy individuals of Delhi, located in Northern India. Out of 309 healthy individuals included in this study, we have found genetic deletion in 21% and 27.4%, GSTM1 and GSTT1 genes, respectively. A small proportion (0.7%) population showed deletion of both the genes. The prevalence of the GSTM1(*)0/0 and GSTT1(*)0/0 genotypes varied within India compared to communities in Chinese, Japanese, Korean and Caucasian.

Challenges establishing a multi-purpose fecal microbiota transplantation stool donor program in Toronto, Canada.

Background: The success of fecal microbiota transplantation (FMT) programs depends on maintaining suitable stool donors. We describe challenges recruiting and retaining universal donors in the first 2 years of an FMT clinical and research program in Toronto and identify opportunities for improvement. Methods: A four-stage screening process is used to identify suitable FMT donors in the Microbiota Therapeutics Outcomes Program. Donor screening follows Health Canada recommendations and excludes persons with history or risk for diseases associated with dysbiosis. Donors are rescreened microbiologically approximately every 1-3 months and answer ongoing health, exposure, and dietary questionnaires. Results: In the first 2 years of our program, 5 of 322 (1.6%) prospective stool donors passed initial screening, and only 2 (0.6%) were retained. Most prospective donors were excluded on telephone screening, at which point high BMI, medication use, and family history of relevant illness were common exclusions. No candidate was excluded because of a concerning physical examination. Microbiologic reasons for donor exclusion included carriage of Blastocystis hominis (n = 2), Helicobacter pylori (n = 2), extended spectrum beta-lactamase producing organisms (n = 1), Shiga-toxin producing Escherichia coli (n = 1), and sapovirus (n = 1). Universal donors were lost temporarily because of travel, antibiotic exposures, and transient carriage of antibiotic-resistant organisms. Conclusions: Recruiting and retaining suitable donors for FMT is challenging because of rigorous exclusions and labour-intensive screening processes. We present considerations for efficiency in donor screening, including targeting recruitment populations, expanded website self-screening, eliminating physical examinations, and streamlining post-travel risk assessment.

Historique: Le succès des programmes de transplantation de microbiote fécal (TMF) dépend de la rétention de donneurs fécaux appropriés. Les auteurs décrivent les difficultés à recruter et à conserver des donneurs universels dans les deux premières années d'un programme clinique et de recherche de TMF à Toronto ainsi qu'à déterminer les possibilités d'amélioration. Méthodologie: Un processus de sélection en quatre étapes permet de déterminer les donneurs de TMF appropriés au sein du programme de résultats thérapeutiques du microbiote. La sélection des donneurs suit les recommandations de Santé Canada et exclut les personnes ayant des antécédents ou un risque de maladies associés à la dysbiose. Les donneurs reprennent une sélection microbiologique environ tous les un à trois mois et répondent à des questionnaires sur la santé, l'exposition et le régime alimentaire. Résultats: Au cours de deux premières années du programme, cinq des 322 donneurs prospectifs de matière fécale (1,6 %) ont réussi la sélection initiale, et seulement deux (0,6 %) ont été retenus. La plupart des donneurs prospectifs ont été exclus à la sélection téléphonique; un IMC élevé, la prise de médicaments et des antécédents familiaux de maladie pertinente étaient des exclusions courantes. Aucun candidat n'a été exclu à cause d'un examen physique inquiétant. Les raisons microbiologiques d'exclure les donneurs incluaient le portage de Blastocystis hominis (n = 2), d'Helicobacter pylori (n = 2), d'organismes producteurs de bêta-lactamase à large spectre (n = 1), d'Escherichia coli producteur de la toxine de Shiga (n = 1) et du sapovirus (n = 1). Des donneurs temporaires étaient perdus temporairement à cause de voyages, d'exposition à des antibiotiques et de portage transitoire d'organismes antibiorésistants. Conclusions: Il est difficile de recruter et de retenir des donneurs appropriés de TMF en raison des exclusions rigoureuses et des processus de dépistage fastidieux. Les auteurs présentent des considérations d'efficacité pour le dépistage des donneurs, y compris le ciblage de populations à recruter, l'autodépistage élargi dans les sites Web, l'élimination des examens physiques et la rationalisation de l'évaluation du risque après le voyage.

Association of CYP1A1, CYP1B1 and CYP17 gene polymorphisms and organochlorine pesticides with benign prostatic hyperplasia.

It is well established that steroidal hormones (testosterone and estrogen) increase benign prostatic hyperplasia (BPH) risk. Cytochrome P450 (CYP) enzymes especially CYP1A1, CYP1B1 and CYP17 metabolize these hormones. Apart from that, several endocrine disrupting organochlorine pesticides (OCPs) are reported to mimic the activity of these steroidal hormones. Therefore, functional polymorphisms in these genes and exposure to such pesticides may increase BPH risk further. Our study included 100 newly diagnosed BPH subjects and 100 age-matched healthy male controls. CYP1A1, CYP1B1 and CYP17 polymorphisms were studied using PCR-RFLP and allele-specific PCR method. OCP levels in blood were analyzed by gas chromatography (GC). Levels of p,p'-DDE and endosulfan α were found to be significantly higher amongst BPH subjects as compared to controls (p-values=0.001 and 0.03 respectively) and CYP17 polymorphism was observed to be significantly associated with BPH subjects as compared to controls (p-values=0.03), indicating that these factors may be important risk factors for BPH. However, further studies are required before unequivocal conclusion.

Association of GSTM1 and GSTT1 polymorphism with lipid peroxidation in benign prostate hyperplasia and prostate cancer: a pilot study.

Association of glutathione S-transferase (GST) M1 and T1 deletions with benign prostate hyperplasia (BPH) and prostate cancer is well reported. These enzymes metabolize numerous toxins thus protecting from oxidative injury. Oxidative stress has been associated with development of BPH and prostate cancer. The present study was designed to analyze role of GST deletions in development of oxidative stress in these subjects. GSTs are responsible for metabolism of toxins present in tobacco therefore effect of tobacco usage in study groups was also studied. Three groups of subjects: BPH (53 patients), prostate cancer (57 patients) and controls (46 subjects) were recruited [corrected]. Genotyping was done using a multiplex polymerase chain reaction (PCR) method. Malondialdehyde (MDA) levels as marker of oxidative stress were estimated by measuring thiobarbituric acid reactive substance (TBARS) in plasma. Based on genotyping, subjects were categorized into: GSTM1+/GSTT1+, GSTM1-/GSTT1+, GSTM1+/GSTT1- and GSTM1-/GSTT1-. Significantly higher plasma MDA levels were noticed in GSTM1-/GSTT1- as compared to GSTM1+/GSTT1+ in all study groups. Double deletion (GSTM1-/GSTT1-) is associated with higher oxidative stress which might play a role in the pathogenesis of BPH and prostate cancer. However, other markers of oxidative stress should be analyzed before any firm conclusion.

DNA damage and cholinesterase activity in occupational workers exposed to pesticides.

The present study was designed to evaluate genotoxicity, acetyl cholinesterase (AChE) activity, hepatic and renal toxicity in occupational workers exposed to mixture of pesticides (n=70) with same number of healthy subjects as controls. The mean comet tail DNA % (TD %) and tail moment (TM) were used to measure DNA damage, while AChE activity and other biochemical parameters such as markers of nephrotoxicity (urea and creatinine) and hepatotoxicity (AST, ALT and ALP) were measured as biomarkers for toxicity due to exposure of pesticides. The occupational workers were continuously exposed to mixture of pirimiphos methyl, chlorpyrifos, temephos and malathion on a regular interval as per usage and activity. The comet assay using lymphocytes of exposed workers showed significantly higher TD percentage value (60.43% vs. 31.86%, p<0.001) and TM value (14.48 µm vs. 6.42 µm, p<0.001) in occupational workers as compared to controls. AChE activity in erythrocytes was found to be decreased (3.45 KAU/L vs. 9.55 KAU/L in controls, p<0.001) and associated with the duration of exposure to pesticides used by the workers. Enzyme levels for hepatic and renal functions were also found significantly different in occupational workers than healthy controls (p<0.001). These results suggest that the exposure to mixture of pirimiphos methyl, chlorpyrifos, temephos and malathion may induce DNA damage, decrease in AChE activity, hepatotoxicity as well as nephrotoxicity. Periodic biomonitoring of these biomarkers along with imparting education and training to occupational workers for safe application of pesticides is recommended for its potential hazards.

CYP 1A1 polymorphism and organochlorine pesticides levels in the etiology of prostate cancer.

Organochlorine pesticides (OCPs) and polymorphisms of xenobiotic metabolizing enzymes are reported to be associated with the possible risk of prostate cancer. OCPs are endocrine disruptors (EDs) which may act by disrupting the physiologic function of endogenous hormones and therefore possibly increase prostate cancer risk. CYP1A1 metabolizes several carcinogens and estrogens, etc. and hence polymorphism of this gene has been reported to be associated with prostate cancer risk. We studied 70 newly diagnosed prostate cancer patients and 61 age-matched healthy male controls. OCP levels in blood were determined by using gas chromatography-mass spectrometry (GC-MS) and CYP1A1 polymorphisms were analyzed by allele-specific PCR and RFLP-PCR methods. Significantly higher levels of ß-HCH, γ-HCH and p,p'-DDE were found in cases as compared to controls (p-values=0.04, 0.008, and 0.01, respectively). Higher levels of γ-HCH were observed in advanced stages of prostate cancer cases (or=T(3)), (p-value=0.04). Dieldrin was found significantly higher in cases with initial stages (p-value=0.03). We did not observe any correlation between prostate cancer and CYP1A1 polymorphisms. Hence, higher level of OCPs, especially ß-HCH, γ-HCH and p,p'-DDE might be associated with prostate cancer risk.

CYP1A1 and CYP3A4 polymorphic variations in Delhi population of Northern India.

Cytochrome P450 (CYP) 1A1 and CYP3A4 are important phase I xenobiotic metabolizing enzymes involved in the metabolism of numbers of toxins, endogenous hormones and pharmaceutical drugs. Polymorphisms in these phase I genes can alter enzyme activity and are known to be associated with cancer susceptibility related to environmental toxins and hormone exposure. Their genotypes may also display ethnicity dependent population frequencies. The present study was aimed to determine the frequencies of commonly known functional polymorphisms of CYP1A1 and CYP3A4 in North Indian population. Allelic frequency of CYP1A1 polymorphisms, m1, m2 and m4 were observed to be 40.3, 31.2 and 0% respectively. Frequency of CYP3A4*1B polymorphism was 0%. We observed inter as well as intra ethnic variation in the distribution of frequency of these polymorphisms. Analysis of polymorphisms in these genes might help in predicting the risk of cancer. Our results emphasize the need for more such studies in "high risk populations".

Frequency of common CYP1B1 polymorphic variations in Delhi population of Northern India.

Cytochrome P4501B1 (CYP1B1) is an extrahepatic enzyme, important in the activation of procarcinogens. It is expressed in steroidegenic tissues and is active in the metabolism of estradiol. CYP1B1 polymorphisms have been shown to be associated with cancer susceptibility related to environmental toxins and hormone exposure. CYP1B1 is also involved in the metabolism of some clinically relevant anticancer drugs. Polymorphisms in the gene have also been associated in primary open-angle glaucoma (POAG). Their genotypes may also display ethnicity dependent population frequencies. Present study was aimed to determine the frequency of five known CYP1B1 polymorphisms in Delhi population. Frequency of CYP1B1 polymorphisms, CYP1B1*2, CYP1B1*3, CYP1B1*4 and CYP1B1*7 were found to be 39, 48.8, 47.3 and 17.07% respectively in normal, healthy individuals. Arg48Gly and Ala119Ser were found to be completely linked with each other. Analysis of CYP1B1 polymorphisms might help in predicting the risk of cancer as well as susceptibility to POAG. Our results emphasize the need for more such studies in "high risk populations".