Environmental estrogen bisphenol A and autoimmunity

Jochmanová, Ivana; Lazurova, Zora; Rudnay, Maroš; Bačová, I.; Mareková, Mária; Lazúrová, Ivica

doi:10.1177/0961203314560205

Cited by 23 publications

(10 citation statements)

References 91 publications

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“…An interesting property of the endocrine disruptors is the occasional stronger effect of low doses, related to the higher ones. Finally, the manifestation of more autoimmune diseases was deduced to the exposure of endocrine disruptors [70,71], and disease susceptibility and its transmission to the progenies also increased [72].…”

Section: Probable Alterations In the Human Lifespan Caused By Modern-mentioning

confidence: 99%

Immunity and longevity

Csaba

2018

AMicr

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The role of immune system is to protect the organism from the not built-in program-like alterations inside and against the agents penetrating from outside (bacteria, viruses, and protozoa). These functions were developed and formed during the evolution. Considering these functions, the immune system promotes the lengthening of lifespan and helps longevity. However, some immune functions have been conveyed by men to medical tools (e.g., pharmaceuticals, antibiotics, and prevention), especially in our modern age, which help the struggle against microbes, but evolutionarily weaken the immune system. Aging is a gradual slow attrition by autoimmunity, directed by the thymus and regulated by the central nervous system and pineal gland. Considering this, thymus could be a pacemaker of aging. The remodeling of the immune system, which can be observed in elderly people and centenarians, is probably not a cause of aging, but a consequence of it, which helps to suit immunity to the requirements. Oxidative stress also helps the attrition of the immune cells and antioxidants help to prolong lifespan. There are gender differences in the aging of the immune system as well as in the longevity. There is an advantage for women in both cases. This can be explained by hormonal differences (estrogens positively influences both processes); however, social factors are also not excluded. The endocrine disruptor chemicals act similar to estrogens, like stimulating or suppressing immunity and provoking autoimmunity; however, their role in longevity is controversial. There are some drugs (rapamycin, metformin, and selegiline) and antioxidants (as vitamins C and E) that prolong lifespan and also improve immunity. It is difficult to declare that longevity is exclusively dependent on the state of the immune system; however, there is a parallelism between the state of immune system and lifespan. It seems likely that there is not a real decline of immunity during aging, but there is a remodeling of the system according to the claims of senescence. This is manifested in the remaining (sometimes stronger) function of memory cells in contrast to the production and number of the new antigen-reactive naive T-cells.

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Section: Probable Alterations In the Human Lifespan Caused By Modern-mentioning

confidence: 99%

Immunity and longevity

Csaba

2018

AMicr

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“…Importantly, such an exposure is now thought to cause various deleterious effects for health (Rochester, 2013;Srivastava et al, 2015). BPA, through acting as a xeno-estrogen (Ben-Jonathan and Steinmetz, 1998), may thus exert reproductive and developmental toxicity (Golub et al, 2010;Peretz et al, 2014); it may also contribute to metabolic and cardiovascular diseases (Lang et al, 2008), may impair immunity (Jochmanova et al, 2015) and is suspected to have carcinogenic properties (Thompson et al, 2015). Such toxic effects have led to governmental restrictive regulations on the production and usage of BPA in North America and the European Union (Birnbaum et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of SLC drug transporter activities by environmental bisphenols

Bruyère

Hubert

Vée

et al. 2017

Toxicology in Vitro

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The plastic component bisphenol A (BPA) is suspected to exert deleterious effects towards human health and targets various cellular and molecular pathways, including activity of ATP-binding cassette drug transporters. The present study was designed to determine whether BPA and some derivatives, like its substitutes bisphenol F (BPF) and bisphenol S (BPS) and the flame retardant tetrabromobisphenol A (TBBPA), may additionally interact with solute carrier (SLC) drug transporters. Activities of the various following SLC transporters were inhibited in a major way (by >60%) by 100μM bisphenols: OCT1 and MATE1 (by BPA and TBBPA), OATP1B1 (by BPA, BPF and TBBPA), OATP1B3 and NTCP (by TBBPA) and OAT3 (by BPA, BPF, BPS and TBBPA); by contrast, activities of other transporters were not impacted (MATE2-K) or were stimulated (notably OCT1 by BPS and OCT2 by BPF). Transporter inhibitions due to bisphenols were concentrations-dependent, with half maximal inhibitory concentrations (IC) ranging from 0.5μM to 73.5μM. BPA was finally shown to be not transported by OAT3, although inhibiting this transporter in a competitive manner. Taken together, these data indicate that bisphenols interact with SLC transporters, at concentration levels however rather higher than those occurring in humans in response to environmental exposure.

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“…Hydrogen peroxide-induced apoptosis and release of autoantigens are consistent with studies showing that estrogen enhances severity and flares of SLE in both human and animal models [57, 58]. Finally, since oxidative stress can be additive, the higher levels of estrogenic hormones in females can also lead to a priming effect, increasing sensitivity to apoptosis from exposure to natural and synthetic compounds with estrogenic activity in the food, soil, air, and water that enter the body via the oral, inhaled, and dermal routes resulting in impaired redox homeostasis [62, 63].…”

Section: A Causal Role For H2o2-induced Apoptosis In the Pathogenementioning

confidence: 99%

Systemic Lupus Erythematosus: Pathogenesis at the Functional Limit of Redox Homeostasis

Pravda¹

2019

Oxidative Medicine and Cellular Longevity

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Systemic lupus erythematosus (SLE) is a disease characterized by the production of autoreactive antibodies and cytokines, which are thought to have a major role in disease activity and progression. Immune system exposure to excessive amounts of autoantigens that are not efficiently removed is reported to play a significant role in the generation of autoantibodies and the pathogenesis of SLE. While several mechanisms of cell death-based autoantigenic exposure and compromised autoantigen removal have been described in relation to disease onset, a significant association with the development of SLE can be attributed to increased apoptosis and impaired phagocytosis of apoptotic cells. Both apoptosis and impaired phagocytosis can be caused by hydrogen peroxide whose cellular production is enhanced by exposure to endogenous hormones or environmental chemicals, which have been implicated in the pathogenesis of SLE. Hydrogen peroxide can cause lymphocyte apoptosis and glutathione depletion, both of which are associated with the severity of SLE. The cellular accumulation of hydrogen peroxide is facilitated by the myriad of stimuli causing increased cellular bioenergetic activity that enhances metabolic production of this toxic oxidizing agent such as emotional stress and infection, which are recognized SLE exacerbating factors. When combined with impaired cellular hydrogen peroxide removal caused by xenobiotics and genetically compromised hydrogen peroxide elimination due to enzymatic polymorphic variation, a mechanism for cellular accumulation of hydrogen peroxide emerges, leading to hydrogen peroxide-induced apoptosis and impaired phagocytosis, enhanced autoantigen exposure, formation of autoantibodies, and development of SLE.

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Environmental estrogen bisphenol A and autoimmunity

Cited by 23 publications

References 91 publications

Immunity and longevity

Immunity and longevity

Inhibition of SLC drug transporter activities by environmental bisphenols

Systemic Lupus Erythematosus: Pathogenesis at the Functional Limit of Redox Homeostasis

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