Can imprinting play a role in the response of<i>Tetrahymena pyriformis</i>to toxic substance exposure?

Nistiar, F; Rácz, Olivér; Brenišin, Marek

doi:10.1093/eep/dvw010

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Treatment of Tetrahymena by it [19] inhibits insulin binding by the receptors and the insulin imprinting induced formation of binding sites but enhances insulin binding in the daughter cell generations. This demonstrates the epigenetic character of the hormonal imprinting at least at a unicellular level [19,40].…”

Section: Hormonal Imprinting At a Unicellular Levelmentioning

confidence: 71%

Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

Csaba

2019

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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.

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Section: Hormonal Imprinting At a Unicellular Levelmentioning

confidence: 71%

Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

Csaba

2019

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“…Descendants of T. pyriformis that survive exposure to a toxic substance became more resistant and the resistance could persist for 1200–1300 generations. This suggests that unicellular organisms can detect toxic molecules and subsequently activate cellular functions so that cells can detoxify and restore themselves 40 …”

Section: Discussionmentioning

confidence: 99%

“…These values were much lower than those in T. pyriformis meaning that T. pyriformis was more resistant to glyphosate than T. thermophila. It is possible that the different IC 50 values obtained in these species may cules and subsequently activate cellular functions so that cells can detoxify and restore themselves 40. T. thermophila is widespread in nature and therefore developed in clean and fresh water.…”

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confidence: 99%

Glyphosate metabolism in Tetrahymena thermophila: A shotgun proteomic analysis approach

Manan

Roytrakul

Charoenlappanit

et al. 2023

Environmental Toxicology

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Glyphosate is one of the most widely used herbicides in the world. However, because of its overuse and resistance to degradation, high levels of glyphosate residues in the environment are reported. Therefore, this study aimed to investigate the effects of glyphosate on proteomic aspects of Tetrahymena thermophila and their uses as bioindicators of freshwater ecosystem. First, an acute toxicity test was performed to determine the median inhibition concentration (IC 50 ). The toxicity test results showed that glyphosate inhibited the growth (proliferation) of T. thermophila. The 96 h-IC 50 value of glyphosate was 171 mg L À1 . No visible changes in aggregation behavior and cell morphology were observed under glyphosate exposure. In addition, the effects of low and high dose glyphosate concentrations (77.5 mg L À1 , 171 mg L À1 ) on the proteomic changes of T. thermophila was investigated using a label-free shotgun proteomic approach. A total of 3191 proteins were identified, 2791 proteins were expressed in the control, 2651 proteins were expressed in 77.5 mg L À1 glyphosates, and 3012 proteins were expressed in 171 mg L À1 glyphosates. Under glyphosate exposure at both low and high dose glyphosate, 400 unique proteins were upregulated. The majority of these proteins was classified as proteins associated with oxidative stress response and intracellular transport indicating the shifts in the internal metabolism. Proteomics revealed that the glyphosate metabolism by T. thermophila is a multi-step process involving several enzymes, which can be divided into four phases, including modification (phase I), conjugation (phase II), transport (phase III), and degradation (phase IV). The accumulation of various biochemical reactions contributes to overall glyphosate resistance. With the proteomics approach, we have found that T. thermophila was equipped with glyphosate detoxification and degradation mechanisms.

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“…The life functions of Tetrahymena are influenced by hormonal imprinting; however, the receptor memory is inclined to slightly decrease after many generations. It is especially interesting that toxic substances in toxic dose can provoke imprinting, which protects later to the effects of imprinter [74]. Such a low dose of 10-18 M, which at the first encounter does not influence the function of the cell, can provoke long-lasting imprinting [75].…”

Section: Receptor Memory and Hormonal Imprintingmentioning

confidence: 99%

Complex multicellular functions at a unicellular eukaryote level: Learning, memory, and immunity

Csaba

2017

Acta Microbiologica et Immunologica Hungarica

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According to experimental data, eukaryote unicellulars are able to learn, have immunity and memory. Learning is carried out in a very primitive form, and the memory is not neural but an epigenetic one. However, this epigenetic memory, which is well justified by the presence and manifestation of hormonal imprinting, is strong and permanent in the life of cell and also in its progenies. This memory is epigenetically executed by the alteration and fixation of methylation pattern of genes without changes in base sequences. The immunity of unicellulars is based on self/non-self discrimination, which leads to the destruction of non-self invaders and utilization of them as nourishment (by phagocytosis). The tools of learning, memory, and immunity of unicellulars are uniformly found in plasma membrane receptors, which formed under the effect of dynamic receptor pattern generation, suggested by Koch et al., and this is the basis of hormonal imprinting, by which the encounter between a chemical substance and the cell is specifically memorized. The receptors and imprinting are also used in the later steps of evolution up to mammals (including man) in each mentioned functions. This means that learning, memory, and immunity can be deduced to a unicellular eukaryote level.

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Can imprinting play a role in the response ofTetrahymena pyriformisto toxic substance exposure?

Cited by 5 publications

References 30 publications

Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

Glyphosate metabolism in Tetrahymena thermophila: A shotgun proteomic analysis approach

Complex multicellular functions at a unicellular eukaryote level: Learning, memory, and immunity

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