TY  - JOUR
AU  - Skalny, Anatoly V.
AU  - Aschner, Michael
AU  - Zhang, Feng
AU  - Guo, Xiong
AU  - Buha-Đorđević, Aleksandra
AU  - Sotnikova, Tatiana I.
AU  - Korobeinikova, Tatiana V.
AU  - Domingo, Jose L.
AU  - Farsky, Sandra H. P.
AU  - Tinkov, Alexey A.
PY  - 2024
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5645
AB  - The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.
PB  - Springer Science and Business Media Deutschland GmbH
T2  - Archives of Toxicology
T1  - Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis
DO  - 10.1007/s00204-024-03772-9
ER  - 

@article{
author = "Skalny, Anatoly V. and Aschner, Michael and Zhang, Feng and Guo, Xiong and Buha-Đorđević, Aleksandra and Sotnikova, Tatiana I. and Korobeinikova, Tatiana V. and Domingo, Jose L. and Farsky, Sandra H. P. and Tinkov, Alexey A.",
year = "2024",
abstract = "The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.",
publisher = "Springer Science and Business Media Deutschland GmbH",
journal = "Archives of Toxicology",
title = "Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis",
doi = "10.1007/s00204-024-03772-9"
}

Skalny, A. V., Aschner, M., Zhang, F., Guo, X., Buha-Đorđević, A., Sotnikova, T. I., Korobeinikova, T. V., Domingo, J. L., Farsky, S. H. P.,& Tinkov, A. A.. (2024). Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis. in Archives of Toxicology
Springer Science and Business Media Deutschland GmbH..
https://doi.org/10.1007/s00204-024-03772-9

Skalny AV, Aschner M, Zhang F, Guo X, Buha-Đorđević A, Sotnikova TI, Korobeinikova TV, Domingo JL, Farsky SHP, Tinkov AA. Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis. in Archives of Toxicology. 2024;.
doi:10.1007/s00204-024-03772-9 .

Skalny, Anatoly V., Aschner, Michael, Zhang, Feng, Guo, Xiong, Buha-Đorđević, Aleksandra, Sotnikova, Tatiana I., Korobeinikova, Tatiana V., Domingo, Jose L., Farsky, Sandra H. P., Tinkov, Alexey A., "Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis" in Archives of Toxicology (2024),
https://doi.org/10.1007/s00204-024-03772-9 . .

TY  - JOUR
AU  - Aschner, Michael
AU  - Skalny, Anatoly
AU  - Santamaria, Abel
AU  - Buha-Đorđević, Aleksandra
AU  - Tizabi, Yousef
AU  - Jiang, Yueming
AU  - Lu, Rongzhu
AU  - Virgolini, Miriam B.
AU  - Tinkov, Alexey A.
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5081
AB  - Titanium dioxide nanoparticles (TiO2NPs) are widely produced and used nanoparticles. Yet, TiO2NP exposure may possess toxic effects to different cells and tissues, including the brain. Recent studies significantly expanded the understanding of the molecular mechanisms underlying TiO2NP neurotoxicity implicating a number of both direct and indirect mechanisms. In view of the significant recent progress in research on TiO2NP neurotoxicity, the objective of the present study is to provide a narrative review on the molecular mechanisms involved in its neurotoxicity, with a special focus on the studies published in the last decade. The existing data demosntrate that although TiO2NP may cross blood-brain barrier and accumulate in brain, its neurotoxic effects may be mediated by systemic toxicity. In addition to neuronal damage and impaired neurogenesis, TiO2NP exposure also results in reduced neurite outgrowth and impaired neurotransmitter metabolism, especially dopamine and glutamate. TiO2NP exposure was also shown to promote α-synuclein and β-amyloid aggregation, thus increasing its toxicity. Recent findings also suggest that epigenetic effects and alterations in gut microbiota biodiversity contribute to TiO2NP neurotoxicity. Correspondingly, in vivo studies demosntrated that TiO2NPs induce a wide spectrum of adverse neurobehavioral effects, while epidemiological data are lacking. In addition, TiO2NPs were shown to promote neurotoxic effects of other toxic compounds. Here we show the contribution of a wide spectrum of molecular mechanisms to TiO2NP-induced neurotoxicity; yet, the role of TiO2NP exposure in adverse neurological outcomes in humans has yet to be fully appreciated.
PB  - IMR Press Limited
T2  - Frontiers in Bioscience - Landmark
T1  - From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles
VL  - 28
IS  - 9
SP  - 1
EP  - 21
DO  - 10.31083/j.fbl2809204
ER  - 

@article{
author = "Aschner, Michael and Skalny, Anatoly and Santamaria, Abel and Buha-Đorđević, Aleksandra and Tizabi, Yousef and Jiang, Yueming and Lu, Rongzhu and Virgolini, Miriam B. and Tinkov, Alexey A.",
year = "2023",
abstract = "Titanium dioxide nanoparticles (TiO2NPs) are widely produced and used nanoparticles. Yet, TiO2NP exposure may possess toxic effects to different cells and tissues, including the brain. Recent studies significantly expanded the understanding of the molecular mechanisms underlying TiO2NP neurotoxicity implicating a number of both direct and indirect mechanisms. In view of the significant recent progress in research on TiO2NP neurotoxicity, the objective of the present study is to provide a narrative review on the molecular mechanisms involved in its neurotoxicity, with a special focus on the studies published in the last decade. The existing data demosntrate that although TiO2NP may cross blood-brain barrier and accumulate in brain, its neurotoxic effects may be mediated by systemic toxicity. In addition to neuronal damage and impaired neurogenesis, TiO2NP exposure also results in reduced neurite outgrowth and impaired neurotransmitter metabolism, especially dopamine and glutamate. TiO2NP exposure was also shown to promote α-synuclein and β-amyloid aggregation, thus increasing its toxicity. Recent findings also suggest that epigenetic effects and alterations in gut microbiota biodiversity contribute to TiO2NP neurotoxicity. Correspondingly, in vivo studies demosntrated that TiO2NPs induce a wide spectrum of adverse neurobehavioral effects, while epidemiological data are lacking. In addition, TiO2NPs were shown to promote neurotoxic effects of other toxic compounds. Here we show the contribution of a wide spectrum of molecular mechanisms to TiO2NP-induced neurotoxicity; yet, the role of TiO2NP exposure in adverse neurological outcomes in humans has yet to be fully appreciated.",
publisher = "IMR Press Limited",
journal = "Frontiers in Bioscience - Landmark",
title = "From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles",
volume = "28",
number = "9",
pages = "1-21",
doi = "10.31083/j.fbl2809204"
}

Aschner, M., Skalny, A., Santamaria, A., Buha-Đorđević, A., Tizabi, Y., Jiang, Y., Lu, R., Virgolini, M. B.,& Tinkov, A. A.. (2023). From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles. in Frontiers in Bioscience - Landmark
IMR Press Limited., 28(9), 1-21.
https://doi.org/10.31083/j.fbl2809204

Aschner M, Skalny A, Santamaria A, Buha-Đorđević A, Tizabi Y, Jiang Y, Lu R, Virgolini MB, Tinkov AA. From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles. in Frontiers in Bioscience - Landmark. 2023;28(9):1-21.
doi:10.31083/j.fbl2809204 .

Aschner, Michael, Skalny, Anatoly, Santamaria, Abel, Buha-Đorđević, Aleksandra, Tizabi, Yousef, Jiang, Yueming, Lu, Rongzhu, Virgolini, Miriam B., Tinkov, Alexey A., "From Mechanisms to Implications: Understanding the Molecular Neurotoxicity of Titanium Dioxide Nanoparticles" in Frontiers in Bioscience - Landmark, 28, no. 9 (2023):1-21,
https://doi.org/10.31083/j.fbl2809204 . .