Endocrine disruptors: Unravelling the link between chemical exposure and Women's reproductive health.

An Endocrine Disrupting Chemical (EDC) is any compound that disrupts the function of the endocrine system in humans and is ubiquitous in the environment either as a result of natural events or through anthropogenic activities. Bisphenol A, phthalates, parabens, pesticides, triclosan, polychlorinated biphenyls, and heavy metals, which are frequently found in the pharmaceutical, cosmetic, and packaging sectors, are some of the major sources of EDC pollutants. EDCs have been identified to have a deteriorating effect on the female reproductive system, as evidenced by the increasing number of reproductive disorders such as endometriosis, uterine fibroids, polycystic ovary syndrome, premature ovarian failure, menstrual irregularity, menarche, and infertility. Studying EDCs in relation to women's health is essential for understanding the complex interactions between environmental factors and health outcomes. It enables the development of strategies to mitigate risks, protect reproductive and overall health, and inform public policy decisions to safeguard women's well-being. Healthcare professionals must know the possible dangers of EDC exposure and ask about environmental exposures while evaluating patients. This may result in more precise diagnosis and personalized treatment regimens. This review summarises the existing understanding of prevalent EDCs that impact women's health and involvement in female reproductive dysfunction and underscores the need for more research. Further insights on potential mechanisms of action of EDCs on female has been emphasized in the article. We also discuss the role of nutritional intervention in reducing the effect of EDCs on women's reproductive health. EDC pollution can be further reduced by adhering to strict regulations prohibiting the release of estrogenic substances into the environment.

Mitigating microplastic pollution: A critical review on the effects, remediation, and utilization strategies of microplastics.

Microplastics are found ubiquitous in the natural environment and are an increasing source of worry for global health. Rapid industrialization and inappropriate plastic waste management in our daily lives have resulted in an increase in the amount of microplastics in the ecosystem. Microplastics that are <150 µm in size could be easily ingested by living beings and cause considerable toxicity. Microplastics can aggregate in living organisms and cause acute, chronic, carcinogenic, developmental, and genotoxic damage. As a result, a sustainable approach to reducing, reusing, and recycling plastic waste is required to manage microplastic pollution in the environment. However, there is still a significant lack of effective methods for managing these pollutants. As a result, the purpose of this review is to convey information on microplastic toxicity and management practices that may aid in the reduction of microplastic pollution. This review further insights on how plastic trash could be converted as value-added products, reducing the load of accumulating plastic wastes in the environment, and leading to a beneficial endeavor for humanity.

Endocrine disrupting chemicals and their effects on the reproductive health in men.

Endocrine Disrupting Chemicals (EDCs) are harmful compounds that enter the environment naturally or through anthropogenic activities and disrupt normal endocrine functions in humans, adversely affecting reproductive health. Among the most significant sources of EDC contaminants are the pharmaceutical, cosmetic, and packaging industries. EDCs have been identified to have a deteriorating effect on male reproductive system, as evidenced by the increasing number of male infertility cases. A large number of case studies have been published in which men exposed to EDCs experienced testicular cancer, undescended testicles, a decrease in serum testosterone levels, and poor semen quality. Furthermore, epidemiological evidence suggested a link between prenatal EDC exposure and cryptorchidism or undescended testicles, hypospadias, and decreased anogenital distance in infants. The majority of these findings, however, are incongruent due to the lack of long-term follow-up studies that would demonstrate EDCs to be associated with male reproductive disorders. This review aims to provide an overview on recent scientific progress on the association of EDCs to male reproductive health with special emphasis on its toxicity and possible mechanism of EDCs that disrupt male reproductive system.

Water a major source of endocrine-disrupting chemicals: An overview on the occurrence, implications on human health and bioremediation strategies.

Endocrine disrupting chemicals (EDCs) are toxic compounds that occur naturally or are the output of anthropogenic activities that negatively impact both humans and wildlife. A number of diseases are associated with these disruptors, including reproductive disorders, cardiovascular disorders, kidney disease, neurological disorders, autoimmune disorders, and cancer. Due to their integral role in pharmaceuticals and cosmetics, packaging companies, agro-industries, pesticides, and plasticizers, the scientific awareness on natural and artificial EDCs are increasing. As these xenobiotic compounds tend to bioaccumulate in body tissues and may also persist longer in the environment, the concentrations of these organic compounds may increase far from their original point of concentrations. Water remains as the major sources of how humans and animals are exposed to EDCs. However, these toxic compounds cannot be completely biodegraded nor bioremediated from the aqueous medium with conventional treatment strategies thereby requiring much more efficient strategies to combat EDC contamination. Recently, genetically engineered microorganism, genome editing, and the knowledge of protein and metabolic engineering has revolutionized the field of bioremediation thereby helping to breakdown EDCs effectively. This review shed lights on understanding the importance of aquatic mediums as a source of EDCs exposure. Furthermore, the review sheds light on the consequences of these EDCs on human health as well as highlights the importance of different remediation and bioremediation approaches. Particular attention is paid to the recent trends and perspectives in order to attain sustainable approaches to the bioremediation of EDCs. Additionally, rigorous restrictions to preclude the discharge of estrogenic chemicals into the environment should be followed in efforts to combat EDC pollution.

Gene-Gene Interactions Reduce Aminoglycoside Susceptibility of Pseudomonas aeruginosa through Efflux Pump-Dependent and -Independent Mechanisms.

Pseudomonas aeruginosa causes a wide range of acute and chronic infections. Aminoglycosides are a cornerstone of treatment, but isolates are often resistant. The purpose of this research was to better understand the genetic basis of aminoglycoside resistance in P. aeruginosa. Bioinformatic approaches identified mutations in resistance-associated genes in the clinical isolates of P. aeruginosa. The common mutations were then engineered into the genome of P. aeruginosa reference strain PAO1. Mutations in the elongation factor gene fusA1 caused the biggest reduction in aminoglycoside susceptibility, with mutations in the two-component regulator gene amgS and the efflux pump regulator gene mexZ having less impact. This susceptibility was further reduced by combinations of mutations. Mutations in fusA1, amgS and mexZ all increased the expression of the mexXY efflux pump that is strongly associated with aminoglycoside resistance. Furthermore, the fusA1 amgS mexZ triple mutant had the highest efflux pump gene expression. Engineering fusA1 and amgS mutants lacking this efflux pump showed that fusA1 and amgS also reduce aminoglycoside susceptibility through additional mechanisms. The fusA1 and amgS mutations reduced bacterial growth, showing that these mutations have a fitness cost. Our findings demonstrate the complex interplay between mutations, efflux pump expression and other mechanisms for reducing the susceptibility of P. aeruginosa to aminoglycosides.

Bioremediation of polycyclic aromatic hydrocarbons: An updated microbiological review.

A class of organic priority pollutants known as PAHs is of critical public health and environmental concern due to its carcinogenic properties as well as its genotoxic, mutagenic, and cytotoxic properties. Research to eliminate PAHs from the environment has increased significantly due to awareness about their negative effects on the environment and human health. Various environmental factors, including nutrients, microorganisms present and their abundance, and the nature and chemical properties of the PAH affect the biodegradation of PAHs. A large spectrum of bacteria, fungi, and algae have ability to degrade PAHs with the biodegradation capacity of bacteria and fungi receiving the most attention. A considerable amount of research has been conducted in the last few decades on analyzing microbial communities for their genomic organization, enzymatic and biochemical properties capable of degrading PAH. While it is true that PAH degrading microorganisms offer potential for recovering damaged ecosystems in a cost-efficient way, new advances are needed to make these microbes more robust and successful at eliminating toxic chemicals. By optimizing some factors like adsorption, bioavailability and mass transfer of PAHs, microorganisms in their natural habitat could be greatly improved to biodegrade PAHs. This review aims to comprehensively discuss the latest findings and address the current wealth of knowledge in the microbial bioremediation of PAHs. Additionally, recent breakthroughs in PAH degradation are discussed in order to facilitate a broader understanding of the bioremediation of PAHs in the environment.

Aminoglycoside-Modifying Enzymes Are Sufficient to Make Pseudomonas aeruginosa Clinically Resistant to Key Antibiotics.

Aminoglycosides are widely used to treat infections of Pseudomonas aeruginosa. Genes encoding aminoglycoside-modifying enzymes (AMEs), acquired by horizontal gene transfer, are commonly associated with aminoglycoside resistance, but their effects have not been quantified. The aim of this research was to determine the extent to which AMEs increase the antibiotic tolerance of P. aeruginosa. Bioinformatics analysis identified AME-encoding genes in 48 out of 619 clinical isolates of P. aeruginosa, with ant(2')-Ia and aac(6')-Ib3, which are associated with tobramcyin and gentamicin resistance, being the most common. These genes and aph(3')-VIa (amikacin resistance) were deleted from antibiotic-resistant strains. Antibiotic minimum inhibitory concentrations (MICs) were reduced by up to 64-fold, making the mutated bacteria antibiotic-sensitive in several cases. Introduction of the same genes into four antibiotic-susceptible P. aeruginosa strains increased the MIC by up to 128-fold, making the bacteria antibiotic-resistant in all cases. The cloned genes also increased the MIC in mutants lacking the MexXY-OprM efflux pump, which is an important contributor to aminoglycoside resistance, demonstrating that AMEs and this efflux pump act independently in determining levels of aminoglycoside tolerance. Quantification of the effects of AMEs on antibiotic susceptibility demonstrates the large effect that these enzymes have on antibiotic resistance.

Aminoglycoside resistance in Pseudomonas aeruginosa: the contribution of the MexXY-OprM efflux pump varies between isolates.

Introduction. Aminoglycoside antibiotics are widely used to treat infections of Pseudomonas aeruginosa. The MexXY-OprM efflux pump is an important contributor to aminoglycoside tolerance in P. aeruginosa reference strains and expression of the mexXY genes is repressed by the MexZ repressor protein. Direct investigation of the role of this efflux pump in clinical isolates is relatively limited.Hypothesis. The contribution of MexXY-OprM to P. aeruginosa aminoglycoside resistance is isolate-specific.Aim. To quantify the role of MexXY-OprM and its repressor, MexZ, in clinical isolates of P. aeruginosa. Methodology. The mexXY genes were deleted from ten clinical isolates of P. aeruginosa, and the mexZ gene from nine isolates. Antimicrobial susceptibility testing was carried out for commonly used antipseudomonal drugs on the engineered mutants and the isogenic wild-type isolates. RT-qPCR was used to measure expression of the mexX gene.Results. All but one of the mexXY mutants were more susceptible to the clinically used aminoglycosides tobramycin, gentamicin and amikacin but the degree to which susceptibility increased varied greatly between isolates. The mexXY mutants were also more susceptible to a fluoroquinolone, ciprofloxacin. In three isolates with functional MexZ, deletion of mexZ increased expression of mexXY and aminoglycoside tolerance. Conversely, deleting mexZ from six clinical isolates with mexZ sequence variants had little or no effect on expression of mexXY or on aminoglycoside susceptibility, consistent with the variants abolishing MexZ function. Genome analysis showed that over 50 % of 619 clinical isolates had sequence variants predicted to reduce the affinity of MexZ for DNA, likely increasing mexXY expression and hence efflux of aminoglycosides.Conclusion. Our findings show that the interplay between MexXY, MexZ and the level of mexXY expression plays an important role in aminoglycoside resistance in clinical isolates of P. aeruginosa but the magnitude of the contribution of this efflux pump to resistance is isolate-specific.