Endocrine Disruptor—A threat to the animal world

Author(s):  
Diptatanu Das ◽  
◽  
Shantanu Das ◽  

Various types of naturally occurring and artificially made chemicals cause disruption of endocrine processes among animals. They mimic biochemically with hormones and interfere with the normal signaling and activity of the endocrine system, causing enormous changes at the cellular level of animals from lower to higher organisms, including human being. These modified regulations of cellular activities as a result of endocrine disruptors have severe implications at the organismal level. Types and adverse effects of these natural and synthetic agents, especially estrogenic compounds causing biological threats have been discussed in details in this review.

2019 ◽  
Vol 20 (6) ◽  
pp. 409-418 ◽  
Author(s):  
György Csaba

Hormonal imprinting takes place perinatally at the first encounter between the developing hormone receptor and its target hormone. This process is needed for the normal function of the receptor- hormone pair and its effect is life-long. However, in this critical period, when the developmental window is open, related molecules (members of the same hormone family, synthetic hormones and hormone-like molecules, endocrine disruptors) also can be bound by the receptor, causing life-long faulty imprinting. In this case, the receptors’ binding capacity changes and alterations are caused at adult age in the sexual and behavioral sphere, in the brain and bones, inclination to diseases and manifestation of diseases, etc. Hereby, faulty hormonal imprinting is the basis of metabolic and immunological imprinting as well as the developmental origin of health and disease (DOHaD). Although the perinatal period is the most critical for faulty imprinting, there are other critical periods as weaning and adolescence, when the original imprinting can be modified or new imprintings develop. Hormonal imprinting is an epigenetic process, without changing the base sequence of DNA, it is inherited in the cell line of the imprinted cells and also transgenerationally (up to 1000 generations in unicellulars and up to the 3rd generation in mammals are justified). Considering the enormously growing number and amount of faulty imprinters (endocrine disruptors) and the hereditary character of faulty imprinting, this latter is threatening the whole human endocrine system.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tatiana Fiordelisio ◽  
Yorgui Santiago ◽  
Itayetzi Romero

Abstract Endocrine disruptors, are chemicals that can alter organism endocrine system. Within these, the heavy metal cadmium is one of the most toxic industrial and environmental metals. Neuroendocrine system act in precise amounts and moments in time, disturbances caused by endocrine disruptors are suspected to be implicated in the recent declining fertility. The effect of cadmium, intraperitoneally injected, on the intracellular calcium activity of gonadotropes was evaluated in an ex vivo preparation of the entire pituitary gland of male BalbC mice by calcium imagenology techniques. In preliminary results, an increase in baseline intracellular calcium activity was observed, as well as an increase in the number of gonadotropes that respond to a GnRH and express gonadotropins. In addition, a change in the pattern of response to GnRH was observed, the biphasic type response being predominant, and an oscillatory depolarization of greater intensity and duration in response to KCl, which is not affected by nifedipine. The results allow us to infer that cadmium affects the function of pituitary gonadotropes and thus probably fertility.


2018 ◽  
Vol 21 (3) ◽  
pp. 161-174 ◽  
Author(s):  
Shanoo Suroowan ◽  
Fawzi Mahomoodally

Background: Common auto-inflammatory disorders (CAIDs) constitute a wide array of ailments ranging from acute allergies to chronic conditions. Globally, CAIDs remain one of the leading causes of disability and morbidity. Despite playing a leading therapeutic role, the vast profusion of anti-inflammatory synthetic agents have not been able to fully resolve a panoply of CAIDs. Additionally, contemporary synthetic therapy approaches remain bounded by a wide array of limitations essentially being adverse effects and unaffordable costs. In this advent, the use of herbal products provides an interesting avenue to explore in view of developing such treatment regimens. Objective: This review article endeavors to highlight potential herbal products and isolated phytochemicals which can be of benefit in the prophylaxis, management, and treatment alongside avoiding the relapse of CAIDs. Conclusion: This review article has highlighted that herbals, herbal products, and isolated metabolites hold a huge potential in the prophylaxis, management, and treatment of CAIDs. Herbals can act on various targets involved in the pathogenesis of inflammatory disorders. In addition, novel approaches for the management of CAIDs are numerous. Indeed, nanoparticles loaded with phytochemicals have been developed to specifically target the colon for IBD treatment. In silico approaches using herbals also offer unlimited avenues to decipher new pharmacophores. Investigating the potential of polyherbal formulations is another unique approach which can be investigated. Given the inefficacy of conventional medicines, the concomitant use of conventional and herbal medicines can also be explored.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
P Dolati ◽  
M J Zamiri ◽  
A Akhlaghi ◽  
Z Jahromi

Abstract Study question Does quercetin (75 or 100 mg/kg BW/day) co-administration with lead acetate to male mice affects embryonic development in female mice? Summary answer The low-dose quercetin (75 mg/kg BW/day) ameliorated the adverse effects of lead acetate on mouse embryogenesis. What is known already Lead causes male infertility by impacting on endocrine system and spermatogenesis, and may exert undesirable effects on the offspring. The currently approved treatment for lead poisoning is the use of chelating agents, which form an insoluble complex with lead and shield it from biological targets; thus, reducing its toxicity. One of the main mechanisms of lead-induced toxicity is oxidative stress, and it has been reported that natural antioxidants can reduce the heavy metals toxicity. The aim of the present study was to examine the protective effects of quercetin on the toxicity induced by lead acetate on the embryogenesis in mice. Study design, size, duration Sexually mature (eight-week-old) NMRI male mice (n = 24) were randomly divided into four groups (n = 6 per group) receiving (i) distilled water (control group); (ii) lead acetate (150 mg/kg BW/day) dissolved in deionized water (LA); (iii) lead acetate (150 mg/kg BW/day) + quercetin (75 mg/kg BW/day) (LQ75); (IV) lead acetate (150 mg/kg BW/day) + quercetin (100 mg/kg BW/day) (LQ100). Treatments were applied daily as oral gavages for one cycle of the seminiferous epithelium (35 days). Participants/materials, setting, methods At the end of treatment administration, the males were joined with super-ovulated females, and the retrieved zygotes were cultured for evaluation of the embryo development (at 2-cell, 4-cell, 8-cell, and blastocyst stages), and blastocyst cell number using differential staining (propidium iodide and bisbenzimide). After incubation of capacitated sperm with oocytes, an ultraviolet light microscope was used following 3 min incubation with 25 µg⁄mL bisbenzamide solution for fertilization assessment. Main results and the role of chance Lead acetate (LA) treatment of male mice decreased the 2-cell stage compared with the control group (P > 0.05). There was no difference between control and LQ75, and between LA and LQ100. The other stages of embryonic development were not significantly affected by the treatment. Overall, early embryonic development in the control and LQ75 mice were better than LQ100 and LA mice. The number of cells in the trophectoderm and inner-cell mass were not affected by treatments. However, the total blastocyst cell number in the control was higher than in the other groups; there was no significant difference between LQ100, LQ75 and LA groups. Fertilization rate was not affected by the treatments (P < 0.05). Quercetin acts as a potent antioxidant at low doses, but at high doses exerts a pro-oxidant action. According to previous reports, higher concentrations of quercetin increased apoptosis and necrosis while decreasing the activities of the antioxidant enzymes. Also, it has been suggested that quercetin might disrupt the endocrine system and interfere with Sertoli cell function and sperm motility. Limitations, reasons for caution A limitation of this study is narrow dose selection; more studies are needed to determine the effective dose of quercetin in ameliorating the lead toxicity. There are also side effects of lead-quercetin chelates such as metal redistribution, essential metal loss, accumulation and persistency in intracellular sites, and peroxidation. Wider implications of the findings: Lead administration adversely impacted on the embryogenesis; on the other hand, paternal quercetin co-administration somewhat ameliorated the adverse effects of lead on mice embryogenesis. Trial registration number Not applicable


Author(s):  
Ninel Shepelska ◽  
Mykola Prodanchuk ◽  
Yana Kolianchuk

Currently, one of the main threats to human health is undoubtedly endocrine disruptors (ED), since they directly disrupt the processes of homeostasis maintenance, controlled by the endocrine system, the purpose of which is to maintain normal functions and development in a constantly changing environment. Pesticides can disrupt the physiological functioning of many endocrine axes, including the endocrine mechanisms that ensure reproductive health. It should be noted that research aimed at preventing chemically induced reproductive disorders in the human population is one of the central areas of preventive medicine, both in terms of their importance and the complexity of the tasks being solved. Analysis and generalization of the results of our own long-term studies have shown that the selective, and, therefore, the most dangerous toxicity of pesticides for the reproductive system is determined by endocrine-mediated mechanisms of etiopathogenesis. The low level of doses inducing pathological changes in reproductive function in our studies fully confirms one of the universal signs inherent in endocrine-distruptive compounds. The above examples demonstrate a wide range of possible endocrine-mediated mechanisms of reproductive toxicity of pesticides - endocrine disruptors. However, it is very important to note that low doses may be more effective in changing some endpoints compared to high (toxic) doses. Currently, several mechanisms have been identified and studied that demonstrate how hormones and ED induce non-monotonic reactions in animal cells, tissues and organs. The reproductive system, the functioning of which is ensured by a fine balancing of the action of androgens and estrogens, is one of the systems that presents a unique opportunity for modeling a non-monotonic dose dependence. All of the above indicates the extreme danger of the impact of hormonally active agents on the reproductive health of a person and his offspring. At the same time, the threat of endocrine-mediated disorders for subsequent generations can also be realized through the induction of mechanisms of development of epigenetic transgenerational effects. Taking into account the results of studies of the mechanisms of the ED destructive action, as well as their ability to induce non-monotonic dose dependence at an extremely low dose level, it should be admitted that, apparently, there is a need to revise the paradigm of methodological approaches to the regulation of pesticides with endocrine-disruptive properties. Key words: pesticides, endocrine disruptors, reproductive system


Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 650 ◽  
Author(s):  
Lisa J. Simpson ◽  
Ellie Tzima ◽  
John S. Reader

Mechanical forces acting on biological systems, at both the macroscopic and microscopic levels, play an important part in shaping cellular phenotypes. There is a growing realization that biomolecules that respond to force directly applied to them, or via mechano-sensitive signalling pathways, can produce profound changes to not only transcriptional pathways, but also in protein translation. Forces naturally occurring at the molecular level can impact the rate at which the bacterial ribosome translates messenger RNA (mRNA) transcripts and influence processes such as co-translational folding of a nascent protein as it exits the ribosome. In eukaryotes, force can also be transduced at the cellular level by the cytoskeleton, the cell’s internal filamentous network. The cytoskeleton closely associates with components of the translational machinery such as ribosomes and elongation factors and, as such, is a crucial determinant of localized protein translation. In this review we will give (1) a brief overview of protein translation in bacteria and eukaryotes and then discuss (2) how mechanical forces are directly involved with ribosomes during active protein synthesis and (3) how eukaryotic ribosomes and other protein translation machinery intimately associates with the mechanosensitive cytoskeleton network.


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