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Commercializing of algal bio-fuel is the major challenge due to proficient harvesting in current scenario. Several species of the algae contain a high concentration of lipids and necessitate simple cultivation methods than usual crops for the conversion of bio-fuels. Algae have the capability to make many biofuels such as bioethanol, biodiesel, bio-hydrogen, etc. Algae bio mass have potential in terms of ‘energy’, but there is challenge in having a feasible balanced energy in algae bio-fuel development operations. Extra challenges of algal harvesting appear from the minute structure of algal cell, comparison of density in the algal cells to the augmentation medium, the pessimistic surface indict on the algal and micro-algae enlargement process which necessitate numerous harvesting compared to the earthbound plants. Centrifugation sedimentation, flotation, filtration and flocculation or a blend of these are main methods of algal harvesting. This paper reviews different methods of harvesting of algae & potential growth of algal biofuel.

Evidence of copper’s (Cu) involvement in Alzheimer’s disease (AD) is available, but information on Cu involvement in microglia and astrocytes during the course of AD has yet to be structurally discussed. This review deals with this matter in an attempt to provide an updated discussion on the role of reactive glia challenged by excess labile Cu in a wide picture that embraces all the major processes identified as playing a role in toxicity induced by an imbalance of Cu in AD.

The present paper deals with the comparative study of performance and emission characteristics of a multicylinder (Indica) engine fueled with Manilkara zapota methyl ester (MZME), Karanja methyl es...

Bacterial secreted proteases are the key factors that increase the virulence potential of different pathogens. Extraintestinal pathogenic E. coli (ExPEC) is a distinct pathotype that has unique ability to infect various body sites apart from the gastrointestinal tract causing several life-threatening diseases both in human and animals. Thus, understanding of ExPEC pathogenesis is crucial in effective management of disease caused by these pathogens. It is known that ExPEC possesses a broad spectrum of virulence factors including the secreted proteases which elude the host defence system. Recent studies have shown that high prevalence as well as the action of the secreted proteases influence the pathogenesis of ExPEC. However, literature on the secreted proteases present in ExPEC and their role in promoting virulence of ExPEC is rather limited. This review describes the distribution, characterization and the role of serine and metalloproteases secreted by diverse pathotypes of ExPEC, highlighting the significance of secreted proteases of ExPEC in pathogenesis.

Clinical heterogeneity is commonly observed in Wilson disease (WD), including cases with identical ATP7B mutations. It is thought to be an outcome of impairment in other genes involved in cellular copper homeostasis in addition to the mutations in the ATP7B gene. ATOX1, a copper chaperone that delivers copper to ATP7B, is a potential genetic modifier of WD. In the present study, we analyzed the genetic variations in the ATOX1 gene in 50 WD patients and 60 controls. We identified four novel variants, of which, the coding region variant c.40G > A, p.(Gly14Ser) was observed in 2% alleles. Interestingly, p.(Gly14Ser) was seen with an early onset age, reduced serum ceruloplasmin level and manifestations of liver and brain in a WD patient unlike the other having identical ATP7B mutation but normal ATOX1 alleles. Further, computational analysis predicted that p.(Gly14Ser) substitution, in the critical copper binding motif (MXCXG14C) of the protein, affects the protein–protein interaction involved in copper sharing and transfer between ATOX1 and ATP7B-MBD4. Our findings suggest that p.(Gly14Ser) variant of ATOX1 might play a role as a genetic modifier leading to phenotypic variation in WD.

Colorectal cancer is one of the leading causes of cancer-related death worldwide. The adenomatous polyposis coli (APC) gene is mutated in hereditary colorectal tumors and in more than 80% of sporadic colorectal tumors. APC mutations impair β-catenin degradation, leading to its permanent stabilization and increased transcription of cancer-driving target genes. In colon cancer, impairment of β-catenin degradation leads to its cytoplasmic accumulation, nuclear translocation, and subsequent activation of tumor cell proliferation. Suppressing β-catenin signaling in cancer cells therefore appears to be a promising strategy for new anticancer strategies. Recently, we discovered a novel Vibrio cholerae cytotoxin, motility-associated killing factor A (MakA), that affects both invertebrate and vertebrate hosts. It promotes bacterial survival and proliferation in invertebrate predators but has unknown biological role(s) in mammalian hosts. Here, we report that MakA can cause lethality of tumor cells via induction of apoptosis. Interestingly, MakA exhibited potent cytotoxic activity, in particular against several tested cancer cell lines, while appearing less toxic toward nontransformed cells. MakA bound to the tumor cell surface became internalized into the endolysosomal compartment and induced leakage of endolysosomal membranes, causing cytosolic release of cathepsins and activation of proapoptotic proteins. In addition, MakA altered β-catenin integrity in colon cancer cells, partly through a caspase- and proteasome-dependent mechanism. Importantly, MakA inhibited β-catenin-mediated tumor cell proliferation. Remarkably, intratumor injection of MakA significantly reduced tumor development in a colon cancer murine solid tumor model. These data identify MakA as a novel candidate to be considered in new strategies for development of therapeutic agents against colon cancer.

Microalgae has a very large diversity compared to any other organism. They are a versatile group of plants that are found almost everywhere such as soil, water, bog and marsh and have evolved over the years to grow and survive in different environments. Most microalgae perform photosynthesis to synthesize food from carbon dioxide and sunlight. However, in the absence of sunlight, to grow and survive they either synthesize their food in the dark environment or feed on organic carbon sources. A number of microalgae species have evolved to feed on organic carbon sources and undergo respiration to facilitate heterotrophic growth. This research focuses on heterotrophic cultivation of algae with wastewater as the growth media and briefly looks at the various cultivation processes with different microalgal strains available. Various additives to instigate the growth of microalgal strains in different cultural mediums are also discussed. This paper can be used as a basis to carry out experiments for a more economical infrastructure.

In the present research work, a promising and underutilized feedstock, Argemone Mexicana (AM) seed oil is converted into biodiesel through the two-step transesterification process using hot plate ma...

Hypnale hypnale (hump-nosed pit viper) is considered to be one among the medically important venomous snake species of India and Sri Lanka. In the present study, venom proteome profiling of a single Hypnale hypnale from Western Ghats of India was achieved using SDS-PAGE based protein separation followed by LC-MS/MS analysis. The identities of the proteins that were not established using the Mascot search were determined through de novo sequencing tools such as Novor followed by MS-BLAST based sequence similarity search algorithm and PEAKS proteomics software. The combined proteomics analysis revealed a total of 37 proteins belonging to nine different snake venom families, in which 7 proteins were exclusively identified through de novo strategies. The enzymatic and non-enzymatic venom protein families identified include serine proteases, metalloproteases, phospholipase A2, thrombin-like enzymes, phospholipase B, C-type lectins/snaclecs, disintegrins, cysteine rich secretory proteins and nerve growth factor. Among these, disintegrins, nerve growth factor, phospholipase B and cysteine rich secretory protein families were identified for the first time in HPV venom. This could possibly explain the regiospecific venom variation seen across snake species. Taken together, the venom proteome profiling on Indian Hypnale hypnale venom correlates with the clinical manifestations often seen in the envenomed victims.

In the present study, the oil extracted from the microalga Neochloris oleoabundans was used for producing biodiesel. The viscosity of microalgal oil was very high so transesterification was done by an ultrasonic method and a simple basic method. Free fatty acid content in oil was found high so a two-step transesterification reaction was used. Maximum yield of algal oil methyl ester was acquired by the ultrasonic method (98%) with improved physicochemical characteristics, whereas the biodiesel yield obtained by simple transesterification process was low (91%). The maximum oil content in N. oleoabundans was found to be 42% and major fatty acids include palmitic acid, oleic acid, and linoleic acid. Finally, it was conferred that the ultrasonic-assisted transesterification method is the best technique for biodiesel production from microalgal oil.

This paper deals with the production of biodiesel using vegetable oil, extracted from Deodar (Cedrus deodara) in various types of ultrasonic reactors. The biodiesel so produced is tested for its property and stability. Biodiesel yield is optimized as a function of reaction time for various ultrasonic reactors. The biodiesel production through the triple-frequency flow cell ultrasonic reactor is found the most energy efficient when compared to other types of ultrasonic reactors. Biodiesel so produced from deodar oil is stable under atmospheric conditions with its various physicochemical properties within the range of acceptable limits of the diesel engine.

Arsenic (As) contamination in rice is at alarming level as majority of rice growing regions are As contaminated such as South East Asia. Restricting the As in aerial parts of rice plant may be an effective strategy to reduce As contamination in food chain. Sulfur (S), an essential element for plant growth and development, plays a crucial role in diminishing heavy metal toxicity. Current study is designed to investigate the role of S to mitigate As toxicity in rice under different S regimes. High S (5 mM) treatment resulted in enhanced root As accumulation as well as prevented its entry in to shoot. Results of thiol metabolism indicate that As was complexed in plant roots through enhanced synthesis of phytochelatins. High S treatment also reduced the expression of OsLsi1 and OsLsi2, the potent transporters of As in rice. High S treatment enhanced the activities of antioxidant enzymes and mitigated the As induced oxidative stress. Thus from present study it is evident that proper supply of S nutrition may be helpful in prevention of As accumulation in aerial parts of plant as well as As induced toxicity.

This study intended to determine whether edible microalgae can play an active role as an anti-virulence agent for enteropathogens. It showed that Chlorella variabilis (ATCC PTA 12198) are able to inhibit the production of the virulence factors in pathogenic Vibrio cholerae strains, the causative agent of cholera cases. Total lipid extract from C. variabilis (TLCV) was able to suppress the cholera toxin (CT) production in multidrug-resistant variant V. cholerae strains without affecting their growth. Cell-cytotoxicity induced by cholera toxin was also arrested in the presence of TLCV. Further, in vivo study in the gut of Artemia salina showed slightly less colonization of V. cholerae in the presence of TLCV. GC-MS analysis of the TLCV revealed the presence of saturated and unsaturated fatty acids include 9-cis,12-cis-Linoleic acid (linoleic acid), 9,12 Octadecadienoic acid (linolenic acid), cis, cis, cis-6,9,12-Octadecatrienoic acid (γ-linolenic acid), cis-8,11,14-Eicosatrienoic acid (dihomo-gamma-linolenic acid) and cis-9-Octadecenoic acid (oleic acid). More specifically the aforesaid formulation works against most recent variant multidrug-resistant V. cholerae strain causing severe diarrhea. Thus, edible microalgae can a valuable natural source which possesses great potential to be developed as functional food ingredients and pharmaceutical products for reducing cholera.

Oxidative stress, characterized by the undue production of reactive oxygen and nitrogen species, is a serious burden in patients having sepsis. SslE, the cell surface associated and secreted lipoprotein with a metalloprotease domain, was identified and found to be widely distributed among the E. coli isolates causing neonatal septicemia. Importantly, SslE was shown to trigger secretion of various proinflammatory cytokines, chemokines, and other proinflammatory hallmarks like reactive oxygen species (ROS) and reactive nitrogen species (RNS) such as NO in mouse macrophages. SslE-induced production of ROS and NO was found to take place via TLR2−/TLR1-dependent manner with the downstream activation of NFκB and MAP kinase signaling molecules. Furthermore, increased expression of MHC II and other co-stimulatory molecules (CD80, CD86) was found on macrophages on induction with SslE, indicating macrophage activation and polarization toward M1 type. Hence, SslE has been identified as one of the factors for inducing production of ROS and NO in macrophages which actually activates host’s innate immune defense against E. coli causing neonatal sepsis, proposing the use of SslE as an immunotherapeutic target against E. coli sepsis. Moreover, identification of the receptor and the signaling pathways for SslE-induced ROS and NO formation would be beneficial to prevent any oxidative stress generated due to SslE in E. coli sepsis.

Copper (Cu) and Iron (Fe) has been the subject of intensive research over several decades as numerous seminal studies robustly support the involvement of Cu and Fe metabolism dyshomeostasis as a common denominator in several neurodegenerative disorders (particularly Alzheimer’s disease and Parkinson’s disease); however, till date, the exact “cause-effect” association has not been elucidated. Thus, there is urgent need to look for newer association/pathways of these redox active elements in different neuropathological conditions. Therefore, in this study, we have used bioinformatics based approach to identify novel Cu and Fe metabolism proteins in neurodegenerative disorders using Cytoscape software. The network biology data demonstrated the association of secreted protein acidic and rich in cysteine (SPARC/osteonectin) protein with Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and neurodegeneration with brain iron accumulation (NBIA) disease, whereas Coagulation factor V may have a role in Brunner Syndrome, Obsessive-Compulsive Disorder, Febrile seizures and Schizophrenia diseases. Further analysis revealed Coagulation factor VII possible role in L1 Syndrome and Congenital hydrocephalus disorders. In conclusion, the present study shows the first evidence in silico that SPARC/osteonectin, Coagulation factor V and VII proteins may have plausible role in the pathogenesis of various neurodegenerative diseases.

A novel activating peptide was designed and synthesized from V. cholerae hemagglutinine protease (HAP) mediated cleavage site of mouse PAR1. The peptide “PFISED” interacts with PAR1 in a new site which is different from its thrombin mediated conventional activation site and induced a series of new downstream signaling pathways. The peptide showed apoptosis in human and mouse breast (MCF-7 and EAC) and colon (HT29 and CT26) cancer cells where as in the same peptide concentration in normal human breast epithelial cells (MCF-10A), normal human fibroblast cells (MRC-5), normal mouse peritoneal macrophage cells and normal mouse breast and colon tissues did not show any effect. Treatment with this peptide enhanced the survival kinetics of EAC induced mice. The peptide mediated apoptosis was inhibited in presence of PAR1 inhibitor and was significantly reduced in si-PAR1 treated cells that indicate the activating peptide “PFISED” induced PAR1 mediated apoptosis of colon and breast cancer cells. This peptide induced over expression and activation of PAR1 and its downstream MAP kinase and NFκB signaling pathways. These signaling pathways enhanced the cellular ROS level to kill malignant cells. We report a novel pro-apoptotic peptide which can selectively kill malignant cells via its specific target receptor PAR1 which is over expressed in the malignant cells and can be used as a molecular target therapy for cancer treatment.

Conventional anticancer therapies are effective but have side effects, so alternative targets are being developed. Bacterial toxins that can kill cells or alter the cellular processes like proliferation, apoptosis and differentiation have been reported for cancer treatment. In this study we have shown antitumor activity of hemagglutinin protease (HAP) secreted by Vibrio cholerae. One µg of HAP showed potent antitumor activity when injected into Ehrlich ascites carcinoma (EAC) tumors in Swiss albino mice. Weekly administration of this dose is able to significantly diminish a large tumor volume within 3 weeks and increases the survival rates of cancerous mice. HAP showed apoptotic activity on EAC and other malignant cells. Increased level of pro-apoptotic p53 with increased ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2 signify that HAP induced apoptogenic signals lead to death of the tumor cells. In vivo and ex vivo studies suggest that mitochondrial dependent intrinsic pathway is responsible for this apoptosis. The level of ROS in malignant cells is reported to be higher than the normal healthy cells. HAP induces oxidative stress and increases the level of ROS in malignant cells which is significantly higher than the normal healthy cells. As a result the malignant cells cross the threshold level of ROS for cell survival faster than normal healthy cells. This mechanism causes HAP mediated apoptosis in malignant cells, but normal cells remain unaltered in the same environment. Our study suggests that HAP may be used as a new candidate drug for cancer therapy.

The current study aimed to identify the selected number of Campylobacter strains of poultry origin in India that were isolated in the Laboratory of International Prevention of Epidemics, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, Japan to the species level with the aid of cdtA/B/C gene-based multiplex PCR assays as well as to investigate their antimicrobial resistance profiles. C. jejuni (4 strains) and C. coli (16 strains) were identified. The poultry isolates identified were subjected to susceptibility testing with the aid of disk diffusion method using 12 antimicrobial agents. Again, the resistant and intermediate isolates confirmed by the disk diffusion method were subjected to determination of minimum inhibitory concentration by agar dilution method. To elucidate the mechanism of quinolone resistance, a total number of 20 quinolone resistant strains were subjected to sequence determination and analysis of the gyrA gene in the quinolone-resistance determining region. The results of the disk diffusion method were consistent with the results of the agar dilution method with slight variation in case of ampicillin, levofloxacin, ofloxacin and fosfomycin. All C. jejuni and C. coli strains had the Thr 86 to Ile substitution in gyrA. Results of this study support the emergence of resistance of C. jejuni and C. coli strains of poultry origin in India to a variety of antimicrobials especially fluoroquinolones. Asian J. Med. Biol. Res. June 2015, 1(1): 1-8

There are numerous genetic factors like MC4R (Melanocortin-4 receptor), POMC (Pro-opiomelanocortin), SIM1 (Single Minded Gene) etc. important in obesity, which can be used as biomarker. But more reliable diagnostic markers are the need for today, along with new therapeutic strategies that target specific molecules in the disease pathways. As in mouse and human genes, where mutations in one or both species are associated with some phenotypic characteristics as observed in human disease. In molecular mechanisms of development, differentiation, and disease gene expression data provide crucial insights. Up-regulation and down-regulation of selective genes can have major effects on diet-induced obesity, but there is little or no effect when animals are fed a low-fat diet. In present study we have studied the gene expression data of mouse at different theiler stages using GXD BioMart. The interacting partners and pathway of the genes that are already used as biomarker in mouse as well as in humans have been studied. A gene NPY1R (Neuropeptide Y1 receptor) was taken as common after STRING and KEGG results on the basis of biochemical pathways and interactions similar to MC4R. Our present work focuses on comparative genomics and proteomics analysis of NPY1R, which has led to identification of biomarker by comparing it with already known MC4R human and mouse biomarker. It has been concluded that both the proteins are structurally and functionally similar.

Malaria, a disease caused by protozoan parasite of the genus Plasmodium, is an ancient enemy of the human race. Despite enormous efforts to control, it is still a main cause of morbidity and mortality in many endemic countries of the world, particularly Africa, South of Sahara. Malaria seems to be unstoppable due to lack of an effective vaccine, acquisition of drug-resistance by malaria parasite, and insecticide resistance by Anopheles mosquitoes. In this scenario, along with search for novel preventive approaches, adequate health facilities, health literacy and awareness among people are required to control and eliminate this formidable disease from society.

The present study was conducted to analyze the expression of urinary proteins in renal cell carcinoma. Morning urine samples were collected from 20 localized clear cell renal cancer patients and 20 healthy age-sex matched controls. Follow-up samples were collected at 12 weeks postnephrectomy. The pooled samples of each group were run on 2-dimensional electrophoresis, gel images were obtained and analyzed. Urinary protein concentration in individual samples of patients with renal cancer (measured using Bradford method) was higher as compared to controls (0.68 ± 0.57 vs 0.33 ± 0.18 mg/ml; p = 0.007).The urinary protein decreased postnephrectomy (p = 0.201). Screening SDS-PAGE showed protein bands with higher intensity (42–70 kDa) in patients with renal cancer. Number of bands was less postoperatively. Master gel image revealed 118 protein spots in renal cancer group, 57 in control and 85 spots postnephrectomy. Abnormal urinary protein expression in patients with clear cell renal cancer can be exploited to look for potential biomarker.

Copper is an essential micronutrient for physiological cell functioning and central nervous system (CNS) development. Indeed, it is a cofactor of many proteins and enzymes in a number of molecular pathways, including energy generation, oxygen transportation, hematopoiesis, cellular growth and metabolism, and signal transduction. This is because it serves as a catalyst of reduction-oxidation (redox) reactions in these processes. When copper is kept under control, bound to special proteins, it yields key properties. However, when it spirals out of control, it is exchanged among small compounds (it is loosely bound to them), and its redox activity makes it dangerous for cell viability, promoting oxidative stress. Copper homeostasis in the CNS is securely synchronized, and perturbations in brain copper levels are known to underlie the pathoetiology of wide spectrum of common neurodegenerative disorders, including Alzheimer's disease. The main objective of this review is to provide some of the most relevant evidence gleaned from recent studies conducted on animal models and humans, and to discuss the evidence as it pertains to a new concept: Aberrant copper metabolism, which appears to have a genetic basis, is a modifiable risk factor accelerating Alzheimer's disease and initiation/progression of cognitive deficits in a percentage of susceptible persons.

Arsenic (As) contamination in rice leads to yield decline and causes carcinogenic risk to human health. Although the role of nitric oxide (NO) in reducing As toxicity is known, NO-mediated genetic modulation in the plant during arsenic toxicity has not yet been established. We analyzed the key components of NO metabolism and the correlations between NO interaction and arsenic stress using rice as a relevant model plant. Illumina sequencing was used to investigate the NO-mediated genome-wide temporal transcriptomic modulation in rice root upon AsIII exposure during 12 days (d) of the growth period. Sodium nitroprusside (SNP) was used as NO donor. SNP supplementation resulted in marked decrease in ROS, cell death and As accumulation during AsIII stress. NO was found to modulate metal transporters particularly NIP, NRAMP, ABC and iron transporters, stress related genes such as CytP450, GSTs, GRXs, TFs, amino acid, hormone(s), signaling and secondary metabolism genes involved in As detoxification. We detected NO-mediated change in jasmonic acid (JA) content during AsIII stress. The study infers that NO reduces AsIII toxicity through modulating regulatory networks involved in As detoxification and JA biosynthesis.

The present study conducted on “Lar stream” which is one of the principal left bank tributaries of the river Jhelum in the Valley of Kashmir (northern India), was an attempt to assess the water quality of the canal by using macro invertebrates present in the ecosystem. During the present study, a total of 26 species of macro invertebrates were registered from Lar stream which belonged to the orders Diptera, Trichoptera, Hirudinae, Ephemeroptera, Plecoptera, Gastropoda, Coleoptera, Arachnida, Lepidoptera, Crustacea, and Oligochaeta. Among all the eleven orders, Dipterans registered a highest of 7 species (27%) and was the most dominant order. Then trend was followed by Trichoptera which registered a total of 5 species (19%) and was the second most dominating group. Similarly, Ephemeroptera, Oligochaeta, Hirudinae, Plecoptera and Gastropoda which registered 2 species (8%) each were the next dominating orders. The least representing taxa were Coleoptera, Arachnida, Lepidoptera and Crustacea which registered only one species (4%) each during the entire study period. The present study concludes that presence of some pollution indicator species such as Tubifex tubifex , Limnodrilus sp. (among Annelida), Chironomous sp., Tabanus sp. etc. (among Arhropoda), Lymnea sp. (among Mollusca) point the changing status of the stream from non-polluted to polluted. DOI: http://dx.doi.org/10.3126/eco.v20i0.11326 Ecoprint An International Journal of Ecology Vol. 20, 2013Page : 19-26

Chronic copper toxicity has been long known to cause hepatotoxicity and liver cirrhosis as observed in Wilson's disease; however, substantial evidence accrued over the time have shown considerable increase in animal studies demonstrating Alzheimer's disease like pathology due to chronic copper-intoxication under certain conditions. This review integrates the contemporary mammalian studies in which the effect of chronic copper intoxication was assessed on the central nervous system and cognition of animals.

The study highlights the role of sulfur (S) in detoxification of arsenate-induced toxicity and the shift in essential element homeostasis in Zea mays L (SRHM 445). Overall growth of arsenate-treated plants under sulfur starvation (−S) was lower than that in the presence of excess sulfur (+S). Translocation of arsenate from roots to shoots, increased under As(−S) and decreased with As(+S). The level of micronutrients (Cu, Zn, Fe) increased in As(−S) plants. Whereas, the level of K and PO4 was higher in As(−S) plants than in As(+S) plants. Higher malondialdehyde, protein carbonyl, and H2O2 levels in As(−S) plants are indicative of higher oxidative stress. Higher superoxide dismutase (SOD) and ascorbate peroxidase (APX) activities, in As(−S) plants coincided with higher H2O2 levels showing the activity of these enzymes are independent of S availability. Absence of reduced glutathione/oxidized glutathione pool in (−S) plants manifested into failure of ascorbate–glutathione detoxification pathway. Hence, S has...

The study empirically evaluates the abatement of As(III) uptake in rice seedlings (7d), in presence of Se and phosphate (P) under hydroponic condition. Positive correlation between As(III) translocation to the shoots of As(III) and P treated seedlings, shows P dependent As(III) translocation in rice. Whereas, presence of both P (5 and 10μgml(-1)) and (0.75μgml(-1)) of Se significantly reduces the As(III) uptake in rice seedlings. Application of Se alone also reduces As(III) uptake both in shoots and roots significantly, however, the seedlings suffers from lipid peroxidation. Among all the studied treatments, lower rates of P (5μgml(-1)) and Se (0.75μgml(-1)) when co-applied, significantly reduced As(III) translocation to the shoots without inflicting much toxicity in the seedlings which is manifested as significant increase in biomass with lower thio-barbituric reactive substances (TBARS). Also, significantly lower TBARS in seedlings receiving As(4)+Se(0.75) and higher TBARS in As(4)+Se(1.5), demonstrates that Se applied at lower rates (0.75μgml(-1)), lowers As induced toxicity. Higher SOD, APX and guaiacol peroxidase (POD) activities in As(4)+P(5)+Se(0.75) compared to that of As(4)+P(5) and As(4)+Se(0.75), supports that lower rate of P and Se provides tolerance towards As induced stress. The nitrogen metabolism in As(4)+P+Se treated seedlings is affected adversely at higher rates of Se and P application. Overall study concluded that application of lower rates of P (5μgml(-1)) and Se (0.75μgml(-1)) provides maximum amelioration of As(III) toxicity in rice seedlings.

Recent therapies of cancer have different side effects, so present scenario demands new therapeutic strategies. Bacterial toxins have been reported to show promising results in cancer treatment. Vibrio cholerae hemagglutinin protease (HAP) regresses tumor growth in Swiss albino mice by programmed cell death of mouse breast cancer cells. Treatment with HAP (one µg/week for three successive weeks) reduced solid tumor and enhanced survival of Ehrlich ascites carcinoma (EAC)-induced Swiss albino mice. A good therapeutic agent should specifically kill malignant cells without any effect on the survival of healthy normal cells. HAP induced PAR1 activation in mouse breast cancer cells (EAC). Overexpression of PAR1 has been reported in different malignant cells when compared to normal cells. HAP-induced PAR1 activated the downstream signaling pathways by nuclear translocation of p50-p65 and the phosphorylation of p38 which caused the activation of NFκB and MAP kinase pathways. The NFκB and MAP kinase activation enhanced the cellular ROS levels. The basal ROS level is reported to be higher in malignant cells as compared to normal healthy cells. Malignant cells cross the threshold level of ROS faster than the normal cells and switch on the cascades of cellular apoptosis. HAP-induced PAR1-mediated apoptosis of malignant cells without altering normal healthy cells makes it a good therapeutic agent for cancer treatment.

Plants are immobile and they have to adapt against adverse conditions of the environment for their survival. Heavy metal (HM) toxicity is posing a serious concern for the plant life and seriously hampering the food grain productivity. Heavy metals include the transition metals essential for plant nutrition as well as the nonessential elements. All these elements become toxic to crop plants when they are present at high tissue concentrations. Elevated concentration of HMs in soil may be due to natural as well as anthropogenic activities. Plants growing in HM-contaminated regions may accumulate a significant amount of these HMs. This paves a way for HMs to enter into food chain posing serious health concerns for animal and human life. A number of morphological, biochemical, and physiological alterations occur during HM toxicity including alteration in uptake mechanism and transportation of water, root and shoot growth, oxidative stress, and changes in HM complexing ligands for sequestration of these HMs into vacuole to reduce the HM concentration in cytoplasm. The present chapter deals with the physiological and biochemical responses of plants to HM toxicity along with shedding light on uptake and transport mechanisms of HMs in brief.

Nitric oxide (NO) and salicylic acid (SA) are important signaling molecules in plant system. In the present study both NO and SA showed a protective role against arsenite (AsIII) stress in rice plants when supplied exogenously. The application of NO and SA alleviated the negative impact of AsIII on plant growth. Nitric oxide supplementation to AsIII treated plants greatly decreased arsenic (As) accumulation in the roots as well as shoots/roots translocation factor. Arsenite exposure in plants decreased the endogenous levels of NO and SA. Exogenous supplementation of SA not only enhanced endogenous level of SA but also the level of NO through enhanced nitrate reductase (NR) activity, whether AsIII was present or not. Exogenously supplied NO decreased the NR activity and level of endogenous NO. Arsenic accumulation was positively correlated with the expression level of OsLsi1, a transporter responsible for AsIII uptake. The endogenous level of NO and SA were positively correlated to each other either when AsIII was present or not. This close relationship indicates that NO and SA work in harmony to modulate the signaling response in AsIII stressed plants.

YghJ, also known as SslE (Secreted and surface associated lipoprotein) is a cell surface associated and secreted lipoprotein harbouring M60 metalloprotease domain. Though the gene is known to be conserved among both pathogenic and commensal Escherichia coli isolates, the expression and secretion of YghJ was found to be higher among diverse E. coli pathotypes. YghJ, secreted from intestinal pathogens such as enterotoxigenic E. coli (ETEC) and enteropathogenic E. coli (EPEC) has been demonstrated to possess mucinase activity and hence facilitates colonization of these enteric pathogens to intestinal epithelial cells. Importantly, YghJ is also reported to be secreted from extraintestinal pathogenic E. coli isolates. In our previous study we have shown that YghJ, purified from a neonatal septicemic E. coli isolate could trigger induction of various proinflammatory cytokines in vitro. This led us to investigate the role of YghJ in causing in vivo tissue hemorrhage. In the present study, we validate the earlier in vitro finding and have showed that YghJ can cause extensive tissue damage in mouse ileum and is also able to induce significant fluid accumulation in a dose dependent manner in a mouse ileal loop (MIL) assay. Hence, our present study not only confirms the pathogenic potential of YghJ in sepsis pathophysiology but also indicates the enterotoxic ability of YghJ which makes it an important virulence determinant of intestinal pathogenic E. coli.

Bacterial toxins have emerged as promising agents in cancer treatment strategy. Hemagglutinin (HAP) protease secreted by Vibrio cholerae induced apoptosis in breast cancer cells and regresses tumor growth in mice model. The success of novel cancer therapies depends on their selectivity for cancer cells with limited toxicity for normal tissues. Increased expression of Protease Activated Receptor-1 (PAR-1) has been reported in different malignant cells. In this study we report that HAP induced activation and over expression of PAR-1 in breast cancer cells (EAC). Immunoprecipitation studies have shown that HAP specifically binds with PAR-1. HAP mediated activation of PAR-1 caused nuclear translocation of p50-p65 and the phosphorylation of p38 which triggered the activation of NFκB and MAP kinase signaling pathways. These signaling pathways enhanced the cellular ROS level in malignant cells that induced the intrinsic pathway of cell apoptosis. PAR-1 mediated apoptosis by HAP of malignant breast cells without effecting normal healthy cells in the same environment makes it a good therapeutic agent for treatment of cancer.

Vibrio cholerae may cause diarrheal diseases and wound infections, both of which have the potential to be fatal. Transmission to humans is often linked to consumption of contaminated shellfish/drin ...

Recent seminal studies have established neurodegeneration, cognitive waning and/or β-amyloid deposition due to chronic copper intoxication via drinking water in healthy animals; henceforth, fuelling the debate all again over the safe levels of copper in the drinking water. This review encompasses the contemporary imperative animal studies in which the effect of chronic copper toxicity (especially via drinking water) was evaluated on the central nervous system and memory of uncompromised animals along with discussing the future perspectives.

We show here that oral immunization with purified outer membrane vesicles (OMVs) of Vibrio cholerae induces a prolonged high rise in the protective antibody titre. Rabbit immune sera were vibriocidal against the homologous and against several heterologous V. cholerae strains in vitro. In addition, OMV immunization conferred significant protective immunity against subsequent bacterial challenges. Thirty OMV-immunized rabbits were challenged with different V. cholerae strains; each challenged group contained five immunized and three unimmunized animals. All the immunized rabbits survived bacterial challenges and were healthy after 24 h, except the two from each group that received the SG24 and SG06 strains, respectively, which developed watery diarrhoea. In contrast, all the unimmunized animals developed cholera-like symptoms, with a death toll of eight within 24 h of challenge. This is the first report of the induction of protective immunity by V. cholerae OMVs in a rabbit model (removable intestinal tie-adult rabbit diarrhoea) that mimics the human disease. Finally, OMVs were found to be significantly less reactogenic than the live and the heat-killed bacteria. Our studies show that oral immunization with OMVs of V. cholerae may induce long-term immunity and may be useful as a 'nonliving' vaccine candidate for the future.

Hypothyroidism during early mammalian brain development is associated with decreased expression of various mitochondrial encoded genes along with evidence for mitochondrial dysfunction. However, in-spite of the similarities between neurological disorders caused by perinatal hypothyroidism and those caused by various genetic mitochondrial defects we still do not know as to how thyroid hormone (TH) regulates mitochondrial transcription during development and whether this regulation by TH is nuclear mediated or through mitochondrial TH receptors? We here in rat cerebellum show that hypothyroidism causes reduction in expression of nuclear encoded genes controlling mitochondrial biogenesis like PGC-1alpha, NRF-1alpha and Tfam. Also, we for the first time demonstrate a mitochondrial localization of thyroid hormone receptor (mTR) isoform in developing brain capable of binding a TH response element (DR2) present in D-loop region of mitochondrial DNA. These results thus indicate an integrated nuclear-mitochondrial cross talk in regulation of mitochondrial transcription by TH during brain development.

Background IP3-mediated calcium mobilization from intracellular stores activates and translocates PKC-α from cytosol to membrane fraction in response to STa in COLO-205 cell line. The present study was undertaken to determine the involvement of cytoskeleton proteins in translocation of PKC-α to membrane from cytosol in the Escherichia coli STa-mediated signaling cascade in a human colonic carcinoma cell line COLO-205. Methods Western blots and consequent densitometric analysis were used to assess time-dependent redistribution of cytoskeletal proteins. This redistribution was further confirmed by using confocal microscopy. Pharmacological reagents were applied to colonic carcinoma cells to disrupt the microfilaments (cytochalasin D) and microtubules (nocodazole). Results STa treatment in COLO-205 cells showed dynamic redistribution and an increase in actin content in the Triton-insoluble fraction, which corresponds to an increase in polymerization within 1 min. Moreover, pharmacological disruption of actin-based cytoskeleton greatly disturbed PKC-α translocation to the membrane. Conclusions These results suggested that the organization of actin cytoskeleton is rapidly rearranged following E. coli STa treatment and the integrity of the actin cytoskeleton played a crucial role in PKC-α movement in colonic cells. Depolymerization of tubulin had no effect on the ability of the kinase to be translocated to the membrane. General significance In the present study, we have shown for the first time that in colonic carcinoma cells, STa-mediated rapid changes of actin cytoskeleton arrangement might be involved in the translocation of PKC-α to membrane.

The 34 kDa major outer membrane protein (MOMP) of Shigella flexneri 2a induces combinatorial expression of TLR2 and TLR6 on peritoneal macrophages of BALB/c mice. Between the two best-characterized TLRs, to date, TLR2 and TLR4, which are chiefly responsible for recognizing majority of bacterial products, TLR2 alone participates in recognition of 34 kDa MOMP. In addition to TLRs, MOMP enhances the mRNA expression of MyD88 and TRAF6 and induces the nuclear translocation of NF-kappaB as well as activates p38 MAP kinase, suggesting the involvement of these molecules in the mechanism of action of MOMP. 34 kDa MOMP also stimulates macrophages, up regulates the surface expression of MHC-II and B7-1 and enhances the production of different cytokines (such as ILp70, TNF-alpha, Il-6) and chemokines (like MIP-1 alpha, MIP-1 beta and RANTES). The ability of the protein in the activation of macrophages, i.e. the induction of nuclear translocation of NF-kappaB and secretion of cytokines are dependent on TLR2 expression as demonstrated by the lack of response by macrophages pre-treated with inhibitory TLR2 mAb. Moreover, it has been found that MOMP induced regulation of TLR2 gene expression is dependent on NF-kappaB and p38 MAP kinase in murine macrophages for the first time. The MOMP induced cytokines and chemokines profile reflect that the protein has the ability to translate innate towards type-1 adaptive response. In conclusion MOMP recognizes by and activates macrophages which may be an initiating event in the antibacterial host response.

This research was conducted to study the growth of Listeria monocytogenes inoculated on frankfurters stored at different conditions as a basis for a safety-based consume by shelf life date label. Three L. monocytogenes strains were separately inoculated at 10 to 20 CFU/cm2 onto frankfurters that were previously formulated with or without high pressure and with or without added 2% potassium lactate (PL) and 0.2% sodium diacetate (SD). Inoculated frankfurters were air or vacuum packaged; stored at 4, 8, or 12 degrees C; and L. monocytogenes and psychrotrophic plate counts were determined for 90, 60, and 45 days, respectively, or until the stationary phase was reached. The data (log CFU per square centimeter versus time) were fitted using the Baranyi-Roberts model to determine maximum growth rates and lag-phase time. The maximum growth rates and the lag time under each growth condition were used to calculate the time to reach 100-fold the initial Listeria population. In frankfurters lacking PL and SD, the count of all strains increased by 2 log after 18 to 50 days at 4 degrees C and 4 to 13 days at 8 degrees C. The growth was inhibited at 4 and 8 degrees C in frankfurters containing PL and SD, but one ribotype was capable of growing, with the time to reach 100-fold the initial Listeria population ranging from 19 to 35 days at 12 degrees C. In most cases, the time to reach 100-fold the initial Listeria population of L. monocytogenes was significantly longer in vacuum-packaged frankfurters as compared with air-packaged samples. Inclusion of PL and SD also inhibited the growth of psychrotrophs, but at all temperatures the psychrotrophic plate counts were greater than 4 log CFU/cm2 at the end of the experiments. These results indicated that despite the use of antimicrobials, certain L. monocytogenes strains could be capable of growing under storage-abuse conditions. Growth kinetics data could be useful for establishing a shelf life date label protocol under different handling scenarios.

The heat-stable enterotoxin (Y-STa) produced by the pathogenic strains of Yersinia enterocolitica is a causative agent of secretory diarrhea. We have reported earlier that Y-STa-induced inositol trisphosphate-mediated cytosolic calcium rise occurs in rat intestinal epithelial cells. In the present communication, the involvement of a nuclear calcium store in the action mechanism of Y-STa in rat intestinal epithelial cells has been shown. Calcium imaging with time series confocal microscopy shows that Y-STa stimulates both the nuclear and cytosolic calcium levels in rat intestinal epithelial cells where a rise in nuclear calcium precedes the cytosolic events. Moreover, Y-STa stimulates both cytosolic and nuclear inositol trisphosphate (IP(3)) levels in a time-dependent manner. Western blot and immunocytochemical analysis reveal a higher density of IP(3) receptor type II in the nuclear membrane compared to the cytosol, which may be the cause of an early rise of the nuclear calcium level. Therefore, it is suggested that Y-STa regulates the nuclear and cytosolic calcium signals in a distinct temporal manner in rat intestinal epithelial cells.

This study compared the performance of four primary mathematical models to study the growth kinetics of Listeria monocytogenes ribotypes grown at low temperature so as to identify the best predictive model. The parameters of the best-fitting model were used to select the fastest growing strains with the shortest lag time and greatest growth rate. Nineteen food, human and animal L. monocytogenes isolates with distinct ribotype were grown at 4, 8, and 12 degrees C in tryptic soy broth and slurries prepared from cooked uncured sliced turkey breasts (with or without potassium lactate and sodium diacetate, PL/SD) and cooked cured frankfurters (with or without PL/SD). Separate regressions were performed on semi-logarithm growth curves to fit linear (based on Monod) and non-linear (Gompertz, Baranyi-Roberts, and Logistic) equations and performance of each model was evaluated using an F-test. No significant differences were found in the performance of linear and non-linear models, but the Baranyi model had the best fit for most growth curves. The maximum growth rate (MGR) of Listeria strains increased with the temperature. Similarly MGR was found significantly greater when no antimicrobials were present in the formulation of turkey or frankfurter products. The variability in lag times and MGRs in all media as determined by the Baranyi model was not consistent among strains. No single strain consistently had the fastest growth (shortest lag time, fastest MGR, or shortest time to increase 100-fold), but nine strains were identified as fastest growing strains under most growth conditions. The lack of association between serotype and fastest strain was also observed in the slurry media study. The fastest growing strains resulting from this study can be recommended for future use in L. monocytogenes challenge studies in delicatessen meat and poultry food matrices, so as to develop conservative pathogen growth predictions.

It was reported earlier that Escherichia coli heat stable enterotoxin (STa), a major causative agent of secretory diarrhea, can also inhibit the proliferation of colon carcinoma cells with the involvement of cGMP mediated calcium influx. In the present study it is shown that E. coli STa inhibits cell proliferation in the colonic carcinoma cell line COLO-205 by the PKG-ERK44/42 mediated signaling pathway. This enterotoxin negatively regulates cell proliferation by downregulating the activity of ERK44/42(MAPK) and subsequently the activity of a transcription regulatory protein cMyc. The antiproliferative effect of STa was reversed by LY83583, a guanylate cyclase (GC) inhibitor and KT5823, a PKG inhibitor. Thus suggesting the involvement of cGMP dependent protein kinase (PKG) in the downregulation of ERK44/42 and subsequent inactivation of cMyc activity. Moreover, it has been shown that a specific ERK44/42 inhibitor, PD98059, also inhibits cMyc activation and cell proliferation, which further confirms the involvement of ERK44/42 in the activation of cMyc. It is also shown that E. coli STa significantly inhibits the vascular endothelial growth factor (VEGF, a potent angiogenic factor) expression in COLO-205 cells and also downregulates vascular cell adhesion molecule-1 (VCAM-1, a potent metastatic factor) expression on the COLO-205 cell surface. So it is reported for the first time that E. coli STa inhibits the proliferation of the colonic carcinoma cell line COLO-205 by the PKG-ERK44/42 mediated pathway and it may have a role against the development of colon carcinoma.

Neonatal sepsis is the invasion of microbial pathogens into blood stream and is associated with a systemic inflammatory response with production and release of a wide range of inflammatory mediators. The increased serum levels of cytokines were found to correlate with the severity and mortality in course of sepsis. There have been no reports on the role of microbial proteases in stimulation of proinflammatory response in neonatal sepsis. We have identified YghJ, a secreted metalloprotease from a neonatal septicemic Escherichia coli (NSEC) isolate. The protease was partially purified from culture supernatant by successive anion and gel filtration chromatography. MS/MS peptide sequencing of the protease showed homology with YghJ. YghJ was cloned, expressed and purified in pBAD TOPO expression vector. YghJ was found to be proteolytically active against Methoxysuccinyl Ala-Ala-Pro-Met-p-nitroanilide oligopeptide substrate, but not against casein and gelatin. YghJ showed optimal activity at pH 7-8 and at temperatures 37-40°C. YghJ showed clear changes in cellular morphologies of Int407, HT-29 and HEK293 cells. YghJ stimulated the secretion of cytokines IL-1α, IL-1β and TNF-α in murine macrophages (RAW 264.7) and IL-8 from human intestinal epithelial cells (HT-29). YghJ also down-regulated the production of anti-inflammatory cytokines such as IL-10. YghJ is present in both septicemic (78%) and fecal E. coli isolates (54%). However, expression and secretion of YghJ is significantly higher among the septicemic (89%) than the fecal isolates (33%). This is the first study to show the role of a microbial protease, YghJ in triggering proinflammatory response in NSEC.

Arsenic (As) contamination of water is a global concern and rice consumption is the biggest dietary exposure to human posing carcinogenic risks, predominantly in Asia. Sulfur (S) is involved in di-sulfide linkage in many proteins and plays crucial role in As detoxification. Present study explores role of variable S supply on rice leaf proteome, its inclination towards amino acids (AA) profile and non protein thiols under arsenite exposure. Analysis of 282 detected proteins on 2-DE gel revealed 113 differentially expressed proteins, out of which 80 were identified by MALDI-TOF-TOF. The identified proteins were mostly involved in glycolysis, TCA cycle, AA biosynthesis, photosynthesis, protein metabolism, stress and energy metabolism. Among these, glycolytic enzymes play a major role in AA biosynthesis that leads to change in AAs profiling. Proteins of glycolytic pathway, photosynthesis and energy metabolism were also validated by western blot analysis. Conclusively S supplementation reduced the As accumulation in shoot positively skewed thiol metabolism and glycolysis towards AA accumulation under AsIII stress.

Proteases in Vibrio cholerae have been shown to play a role in its pathogenesis. V. cholerae secretes Zn-dependent hemagglutinin protease (HAP) and calcium-dependent trypsin-like serine protease (VesC) by using the type II secretion system (TIISS). Our present studies demonstrated that these proteases are also secreted in association with outer membrane vesicles (OMVs) and transported to human intestinal epithelial cells in an active form. OMV-associated HAP induces dose-dependent apoptosis in Int407 cells and an enterotoxic response in the mouse ileal loop (MIL) assay, whereas OMV-associated VesC showed a hemorrhagic fluid response in the MIL assay, necrosis in Int407 cells, and an increased interleukin-8 (IL-8) response in T84 cells, which were significantly reduced in OMVs from VesC mutant strain. Our results also showed that serine protease VesC plays a role in intestinal colonization of V. cholerae strains in adult mice. In conclusion, our study shows that V. cholerae OMVs secrete biologically active proteases which may play a role in cytotoxic and inflammatory responses.

Porphyromonas gingivalis is an anerobic, gram negative, bacterium which is a natural inhabitant of oral microbiome. Under unhealthy oral hygiene conditions the bacterium becomes highly destructive (photobiont) and leads to periodontitis (inflammation of periodontium). Several drugs like chlorhexidine, monocycline effectively reduce the viability of biofilms formed by Porphyromonas gingivalis but, it is impossible to destroy biofilms completely. As the bacterium evolves continuously it develops drug resistance due to events like horizontal gene transfer and its biofilm mode of living. Therefore no drug is very efficient in treating Periodontitis. We have done an Insilco Synteny based comparative analysis to find a druggable target which remains unchanged in various Porphyromonas gingivalis strains. Dipeptidylaminopeptidase has been identified one such potential target which is responsible for virulence in Porphyromonas gingivalis, and is functionally and structurally conserved. Therefore, according to best knowledge of authors a drug developed against this target will be effective in treating periodontitis caused by all evolved forms of bacterium.

Arsenic (As) is posing serious health concerns in South East Asia where rice, an efficient accumulator of As, is prominent crop. Salicylic acid (SA) is an important signalling molecule and plays a crucial role in resistance against biotic and abiotic stress in plants. In present study, ameliorative effect of SA against arsenate (AsV) toxicity has been investigated in rice (Oryza sativa L.). Arsenate stress hampered the plant growth in terms of root, shoots length and biomass as well as it enhanced the level of H2O2 and MDA in dose dependent manner in shoot. Exogenous application of SA, reverted the growth and oxidative stress caused byAsV and significantly decreased As translocation to the shoots. Level of As in shoot was positively correlated with the expression of OsLsi2, efflux transporter responsible for root to shoot translocation of arsenic in the form of arsenite (AsIII). Salicylic acid also overcame AsV induced oxidative stress and modulated the activities of antioxidant enzymes in a differential manner in shoots. Arsenic treatment hampered the translocation of Fe in the shoot which was compensated by the SA treatment. The level of Fe in root and shoot was positively correlated with the transcript level of transporters responsible for the accumulation of Fe,OsNRAMP5 and OsFRDL1, in the root and shoot respectively. Co-application of SA was more effective than pre-treatment for reducing As accumulation as well as imposed toxicity.

The activity of the calcium- and phospholipid-dependent enzyme protein kinase C (PKC) in response to heat-stable enterotoxin (NAG-ST) of Vibrio cholerae non-O1 was examined in isolated rat enterocytes. Optimal stimulation of the membrane-bound PKC activity (about 4.3-fold) was observed after 1 min of incubation of cells with 10 ng/ml toxin; and the effects were dose dependent. Following NAG-ST treatment an increase in PKC activity in the membrane fraction was found with a concomitant decrease in the cytosolic fraction suggesting the redistribution of the enzyme. The pronounced enzyme activity in presence of a classical pseudosubstrate and its complete inhibition by Go 6976 suggested the involvement of a calcium-dependent isoform of PKC (PKC-α). A time course study employing an immunoblot assay provided evidence that NAG-ST led to almost complete translocation of PKC-α to the membrane. A 65% inhibition of enzyme activity in the membrane fraction and inhibition of its translocation to some extent by dantrolene treatment further suggested that the enzyme was translocated with the rise of intracellular calcium ([Ca 2+ ]i). The phosphorylation of three membrane proteins by toxin-induced PKC in vitro and abolition of this phosphorylation by Go 6976 demonstrated that phosphorylation of these membrane proteins was PKC-α mediated and might be involved in the alteration of membrane functions.

Among the indispensable trace elements required for normal physiological growth and development of the body; Copper (Cu) and Selenium (Se) have a paramount significance in human reproduction. Male testosterone levels have been suggested to play a role in the severity of Cu deficiency. In females, estrogen causes increase in plasma Cu levels by inducing ceruloplasmin and alteration of hepatic subcellular distribution of Cu. Thus, changes in Cu levels due to estrogen are thought to protect Cu-deficient females against mortality. During pubertal maturation, the Se content of male gonads increases and it is localized in the mitochondrial capsule protein of the mid-piece. In females, infertility and abortion aberrations are caused due to Se deficiency.