Mitochondrial response and resilience to anthropogenic chemicals during embryonic development

Babich, Remy; Hamlin, Heather J.; Thayer, LeeAnne; Dorr, Madeline; Zheng, Wei; Neilson, Andrew P.; Jayasundara, Nishad

doi:10.1016/j.cbpc.2020.108759

Cited by 5 publications

(4 citation statements)

References 27 publications

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“…Non-monotonic dose response effects and mitochondrial hormesis were detected with some chemicals. The authors conclude that mitochondrial responses to chemicals are highly dynamic and warrant careful consideration when determining the mitochondrial toxicity of a given chemical [144].…”

Section: Discussionmentioning

confidence: 99%

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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A dose-response relationship to stressors, according to the hormesis theory, is characterized by low-dose stimulation and high-dose inhibition. It is non-linear with a low-dose optimum. Stress responses by cells lead to adapted vitality and fitness. Physical stress can be exerted through heat, radiation, or physical exercise. Chemical stressors include reactive species from oxygen (ROS), nitrogen (RNS), and carbon (RCS), carcinogens, elements, such as lithium (Li) and silicon (Si), and metals, such as silver (Ag), cadmium (Cd), and lead (Pb). Anthropogenic chemicals are agrochemicals (phytotoxins, herbicides), industrial chemicals, and pharmaceuticals. Biochemical stress can be exerted through toxins, medical drugs (e.g., cytostatics, psychopharmaceuticals, non-steroidal inhibitors of inflammation), and through fasting (dietary restriction). Key-lock interactions between enzymes and substrates, antigens and antibodies, antigen-presenting cells, and cognate T cells are the basics of biology, biochemistry, and immunology. Their rules do not obey linear dose-response relationships. The review provides examples of biologic stressors: oncolytic viruses (e.g., immuno-virotherapy of cancer) and hormones (e.g., melatonin, stress hormones). Molecular mechanisms of cellular stress adaptation involve the protein quality control system (PQS) and homeostasis of proteasome, endoplasmic reticulum, and mitochondria. Important components are transcription factors (e.g., Nrf2), micro-RNAs, heat shock proteins, ionic calcium, and enzymes (e.g., glutathion redox enzymes, DNA methyltransferases, and DNA repair enzymes). Cellular growth control, intercellular communication, and resistance to stress from microbial infections involve growth factors, cytokines, chemokines, interferons, and their respective receptors. The effects of hormesis during evolution are multifarious: cell protection and survival, evolutionary flexibility, and epigenetic memory. According to the hormesis theory, this is true for the entire biosphere, e.g., archaia, bacteria, fungi, plants, and the animal kingdoms.

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Section: Discussionmentioning

confidence: 99%

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Schirrmacher¹

2021

Biomedicines

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“…PFOS was also frequently detected above sensitive thresholds (LOECs: 3.5 ng/L and 30–100 ng/L) in freshwater samples analyzed here (Figure B). Notably, the nominal concentration in the toxicity experiment was 100 ng/L; however, it was measured at 30 ng/L before the concentration was renewed on day 2 .…”

Section: Resultsmentioning

confidence: 66%

“…PFOA may also be present in river sediments, which can be long-term sources. PFOA was frequently detected in concentrations above the reported LOECs of 3.4 ng/L, 3.5 ng/L, and 200 ng/L − ,, in several locations (Figure A). These LOECs vary due to the different exposure routes and concentrations, as detailed in each study.…”

Section: Resultsmentioning

confidence: 82%

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Estimated Influent PFAS Loads to Wastewater Treatment Plants and Ambient Concentrations in Downstream Waterbodies: Case Study in Southern and Central California

Desgens-Martin

Medina

et al. 2023

ACS EST Water

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Per-and polyfluoroalkyl substances (PFAS) have received increased scrutiny from environmental and public health protection agencies, with focus placed on phased-out "legacy" PFAS such as perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA). However, recent studies highlight the need to also evaluate the risks of replacement and breakdown products such as perfluorobutanesulfonic acid (PFBS) and hexafluoropropylene oxide dimer acid (HFPO-DA). Thus, the objective was to evaluate the ecological risks of legacy and newer PFAS, using monitoring and predictive models. Here, PFBS, PFOA, PFOS, and other PFAS were detected in samples collected downstream from 16 Southern and Central California wastewater treatment plants (WWTPs). PFBS, PFOA, and PFOS were sometimes detected at concentrations above experimentally determined lowest observed effect concentrations. Additionally, ChemFate, a fate and transport model, was used to estimate daily loads to the upstream WWTPs. Population size and urban land use were the best predictors of PFAS loads to WWTPs. The sum of influent loads of selected PFAS was estimated to be 61,000 ± 40,000 kg/year for California. Additionally, the sum of PFAS totaled annually in evaluated regions correlated well with the overall pollution burden. Here, the practicality of using predictive models in conjunction with field sampling to predict PFAS inputs and their ecological risks to the environment was demonstrated.

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Epigenetic Mechanisms of Toxicant-Induced Renal Injury

Kolli,

Jayasundara

2024

Reference Module in Biomedical Sciences

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Mitochondrial response and resilience to anthropogenic chemicals during embryonic development

Cited by 5 publications

References 27 publications

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Less Can Be More: The Hormesis Theory of Stress Adaptation in the Global Biosphere and Its Implications

Estimated Influent PFAS Loads to Wastewater Treatment Plants and Ambient Concentrations in Downstream Waterbodies: Case Study in Southern and Central California

Epigenetic Mechanisms of Toxicant-Induced Renal Injury

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