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 . .

TY  - JOUR
AU  - Baralić, Katarina
AU  - Javorac, Dragana
AU  - Marić, Đurđica
AU  - Đukić-Ćosić, Danijela
AU  - Bulat, Zorica
AU  - Antonijević-Miljaković, Evica
AU  - Anđelković, Milena
AU  - Antonijević, Biljana
AU  - Aschner, Michael
AU  - Buha-Đorđević, Aleksandra
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4351
AB  - The main objective of this research was to conduct a dose–response modeling between the internal dose of measured blood Cd, As, Hg, Ni, and Cr and hormonal response of serum testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). The study included 207 male participants from subjects of 5 different cohorts (patients with prostate, testicular, and pancreatic cancer, patients suffering from various thyroid and metabolic disorders, as well as healthy volunteers), enrolled from January 2019 to May 2021 at the Clinical Centre of Serbia in Belgrade, Serbia. Benchmark dose–response modeling analysis was performed with the PROAST software version 70.1, showing the hormone levels as quantal data. The averaging technique was applied to compute the Benchmark dose (BMD) interval (BMDI), with benchmark response set at 10%. Dose-response relationships between metal/metalloid blood concentration and serum hormone levels were confirmed for all the investigated metals/metalloid and hormones. The narrowest BMDI was found for Cd-testosterone and Hg-LH pairs, indicative of high confidence in these estimates. Although further research is needed, the observed findings demonstrate that the BMD approach may prove to be significant in the dose–response modeling of human data.
PB  - Elsevier B.V.
T2  - Environment International
T1  - Benchmark dose approach in investigating the relationship between blood metal levels and reproductive hormones: Data set from human study
VL  - 165
DO  - 10.1016/j.envint.2022.107313
ER  - 

@article{
author = "Baralić, Katarina and Javorac, Dragana and Marić, Đurđica and Đukić-Ćosić, Danijela and Bulat, Zorica and Antonijević-Miljaković, Evica and Anđelković, Milena and Antonijević, Biljana and Aschner, Michael and Buha-Đorđević, Aleksandra",
year = "2022",
abstract = "The main objective of this research was to conduct a dose–response modeling between the internal dose of measured blood Cd, As, Hg, Ni, and Cr and hormonal response of serum testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). The study included 207 male participants from subjects of 5 different cohorts (patients with prostate, testicular, and pancreatic cancer, patients suffering from various thyroid and metabolic disorders, as well as healthy volunteers), enrolled from January 2019 to May 2021 at the Clinical Centre of Serbia in Belgrade, Serbia. Benchmark dose–response modeling analysis was performed with the PROAST software version 70.1, showing the hormone levels as quantal data. The averaging technique was applied to compute the Benchmark dose (BMD) interval (BMDI), with benchmark response set at 10%. Dose-response relationships between metal/metalloid blood concentration and serum hormone levels were confirmed for all the investigated metals/metalloid and hormones. The narrowest BMDI was found for Cd-testosterone and Hg-LH pairs, indicative of high confidence in these estimates. Although further research is needed, the observed findings demonstrate that the BMD approach may prove to be significant in the dose–response modeling of human data.",
publisher = "Elsevier B.V.",
journal = "Environment International",
title = "Benchmark dose approach in investigating the relationship between blood metal levels and reproductive hormones: Data set from human study",
volume = "165",
doi = "10.1016/j.envint.2022.107313"
}

Baralić, K., Javorac, D., Marić, Đ., Đukić-Ćosić, D., Bulat, Z., Antonijević-Miljaković, E., Anđelković, M., Antonijević, B., Aschner, M.,& Buha-Đorđević, A.. (2022). Benchmark dose approach in investigating the relationship between blood metal levels and reproductive hormones: Data set from human study. in Environment International
Elsevier B.V.., 165.
https://doi.org/10.1016/j.envint.2022.107313

Baralić K, Javorac D, Marić Đ, Đukić-Ćosić D, Bulat Z, Antonijević-Miljaković E, Anđelković M, Antonijević B, Aschner M, Buha-Đorđević A. Benchmark dose approach in investigating the relationship between blood metal levels and reproductive hormones: Data set from human study. in Environment International. 2022;165.
doi:10.1016/j.envint.2022.107313 .

Baralić, Katarina, Javorac, Dragana, Marić, Đurđica, Đukić-Ćosić, Danijela, Bulat, Zorica, Antonijević-Miljaković, Evica, Anđelković, Milena, Antonijević, Biljana, Aschner, Michael, Buha-Đorđević, Aleksandra, "Benchmark dose approach in investigating the relationship between blood metal levels and reproductive hormones: Data set from human study" in Environment International, 165 (2022),
https://doi.org/10.1016/j.envint.2022.107313 . .

TY  - JOUR
AU  - Aaseth, Jan
AU  - Javorac, Dragana
AU  - Buha-Đorđević, Aleksandra
AU  - Bulat, Zorica
AU  - Skalny, Anatoly
AU  - Zaitseva, Irina
AU  - Aschner, Michael
AU  - Tinkov, Alexey
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4059
AB  - Persistent organic pollutants (POPs) are considered as potential obesogens that may affect adipose tissue development and functioning, thus promoting obesity. However, various POPs may have different mechanisms of action. The objective of the present review is to discuss the key mechanisms linking exposure to POPs to adipose tissue dysfunction and obesity. Laboratory data clearly demonstrate that the mechanisms associated with the interference of exposure to POPs with obesity include: (a) dysregulation of adipogenesis regulators (PPAR  and C/EBP); (b) affinity and binding to nuclear receptors; (c) epigenetic effects; and/or (d) proinflammatory activity. Although in vivo data are generally corroborative of the in vitro results, studies in living organisms have shown that the impact of POPs on adipogenesis is affected by biological factors such as sex, age, and period of exposure. Epidemiological data demonstrate a significant association between exposure to POPs and obesity and obesity-associated metabolic disturbances (e.g., type 2 diabetes mellitus and metabolic syndrome), although the existing data are considered insufficient. In conclusion, both laboratory and epidemiological data underline the significant role of POPs as environmental obesogens. However, further studies are required to better characterize both the mechanisms and the dose/concentration-response effects of exposure to POPs in the development of obesity and other metabolic diseases.
PB  - MDPI
T2  - Toxics
T1  - The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies
VL  - 10
IS  - 2
DO  - 10.3390/toxics10020065
ER  - 

@article{
author = "Aaseth, Jan and Javorac, Dragana and Buha-Đorđević, Aleksandra and Bulat, Zorica and Skalny, Anatoly and Zaitseva, Irina and Aschner, Michael and Tinkov, Alexey",
year = "2022",
abstract = "Persistent organic pollutants (POPs) are considered as potential obesogens that may affect adipose tissue development and functioning, thus promoting obesity. However, various POPs may have different mechanisms of action. The objective of the present review is to discuss the key mechanisms linking exposure to POPs to adipose tissue dysfunction and obesity. Laboratory data clearly demonstrate that the mechanisms associated with the interference of exposure to POPs with obesity include: (a) dysregulation of adipogenesis regulators (PPAR  and C/EBP); (b) affinity and binding to nuclear receptors; (c) epigenetic effects; and/or (d) proinflammatory activity. Although in vivo data are generally corroborative of the in vitro results, studies in living organisms have shown that the impact of POPs on adipogenesis is affected by biological factors such as sex, age, and period of exposure. Epidemiological data demonstrate a significant association between exposure to POPs and obesity and obesity-associated metabolic disturbances (e.g., type 2 diabetes mellitus and metabolic syndrome), although the existing data are considered insufficient. In conclusion, both laboratory and epidemiological data underline the significant role of POPs as environmental obesogens. However, further studies are required to better characterize both the mechanisms and the dose/concentration-response effects of exposure to POPs in the development of obesity and other metabolic diseases.",
publisher = "MDPI",
journal = "Toxics",
title = "The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies",
volume = "10",
number = "2",
doi = "10.3390/toxics10020065"
}

Aaseth, J., Javorac, D., Buha-Đorđević, A., Bulat, Z., Skalny, A., Zaitseva, I., Aschner, M.,& Tinkov, A.. (2022). The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies. in Toxics
MDPI., 10(2).
https://doi.org/10.3390/toxics10020065

Aaseth J, Javorac D, Buha-Đorđević A, Bulat Z, Skalny A, Zaitseva I, Aschner M, Tinkov A. The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies. in Toxics. 2022;10(2).
doi:10.3390/toxics10020065 .

Aaseth, Jan, Javorac, Dragana, Buha-Đorđević, Aleksandra, Bulat, Zorica, Skalny, Anatoly, Zaitseva, Irina, Aschner, Michael, Tinkov, Alexey, "The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies" in Toxics, 10, no. 2 (2022),
https://doi.org/10.3390/toxics10020065 . .

TY  - JOUR
AU  - Tinkov, Alexey
AU  - Nguyen, Thuy
AU  - Santamaria, Abe
AU  - Bowman, Aaron
AU  - Buha-Đorđević, Aleksandra
AU  - Paoliello, Monica Maria
AU  - Skalny, Anatoly
AU  - Aschner, Michael
PY  - 2021
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3910
AB  - Metal dyshomeostasis, and especially overexposure, is known to cause adverse health effects due to modulation of a variety of metabolic pathways. An increasing body of literature has demonstrated that metal exposure may affect SIRT signaling, although the existing data are insufficient. Therefore, in this review we discuss the available data (PubMed-Medline, Google Scholar) on the influence of metal overload on sirtuin (SIRT) signaling and its association with other mechanisms involved in metal-induced toxicity. The existing data demonstrate that cadmium (Cd), mercury (Hg), arsenic (As), lead (Pb), aluminium (Al), hexavalent chromium (CrVI), manganese (Mn), iron (Fe), and copper (Cu) can inhibit SIRT1 activity. In addition, an inhibitory effect of Cd, Pb, As, and Fe on SIRT3 has been demonstrated. In turn, metal-induced inhibition of SIRT was shown to affect deacetylation of target proteins including FOXO, PGC1α, p53 and NF-kB. Increased acetylation downregulates PGC1α signaling pathway, resulting in cellular altered redox status and increased susceptibility to oxidative stress, as well as decreased mitochondrial biogenesis. Lower rates of LKB1 deacetylation may be responsible for metal-induced decreases in AMPK activity and subsequent metabolic disturbances. A shift to the acetylated FOXO results in increased expression of pro-apoptotic genes which upregulates apoptosis together with increased p53 signaling. Correspondingly, decreased NF-kB deacetylation results in upregulation of target genes of proinflammatory cytokines, enzymes, and cellular adhesion molecules thus promoting inflammation. Therefore, alterations in sirtuin activity may at least partially mediate metal-induced metabolic disturbances that have been implicated in neurotoxicity, nephrotoxicity, cardiotoxicity, and other toxic effects of heavy metals.
PB  - Springer
T2  - Archives of Toxicology
T1  - Sirtuins as molecular targets, mediators, and protective agents in metal‑induced toxicity
DO  - 10.1007/s00204-021-03048-6
ER  - 

@article{
author = "Tinkov, Alexey and Nguyen, Thuy and Santamaria, Abe and Bowman, Aaron and Buha-Đorđević, Aleksandra and Paoliello, Monica Maria and Skalny, Anatoly and Aschner, Michael",
year = "2021",
abstract = "Metal dyshomeostasis, and especially overexposure, is known to cause adverse health effects due to modulation of a variety of metabolic pathways. An increasing body of literature has demonstrated that metal exposure may affect SIRT signaling, although the existing data are insufficient. Therefore, in this review we discuss the available data (PubMed-Medline, Google Scholar) on the influence of metal overload on sirtuin (SIRT) signaling and its association with other mechanisms involved in metal-induced toxicity. The existing data demonstrate that cadmium (Cd), mercury (Hg), arsenic (As), lead (Pb), aluminium (Al), hexavalent chromium (CrVI), manganese (Mn), iron (Fe), and copper (Cu) can inhibit SIRT1 activity. In addition, an inhibitory effect of Cd, Pb, As, and Fe on SIRT3 has been demonstrated. In turn, metal-induced inhibition of SIRT was shown to affect deacetylation of target proteins including FOXO, PGC1α, p53 and NF-kB. Increased acetylation downregulates PGC1α signaling pathway, resulting in cellular altered redox status and increased susceptibility to oxidative stress, as well as decreased mitochondrial biogenesis. Lower rates of LKB1 deacetylation may be responsible for metal-induced decreases in AMPK activity and subsequent metabolic disturbances. A shift to the acetylated FOXO results in increased expression of pro-apoptotic genes which upregulates apoptosis together with increased p53 signaling. Correspondingly, decreased NF-kB deacetylation results in upregulation of target genes of proinflammatory cytokines, enzymes, and cellular adhesion molecules thus promoting inflammation. Therefore, alterations in sirtuin activity may at least partially mediate metal-induced metabolic disturbances that have been implicated in neurotoxicity, nephrotoxicity, cardiotoxicity, and other toxic effects of heavy metals.",
publisher = "Springer",
journal = "Archives of Toxicology",
title = "Sirtuins as molecular targets, mediators, and protective agents in metal‑induced toxicity",
doi = "10.1007/s00204-021-03048-6"
}

Tinkov, A., Nguyen, T., Santamaria, A., Bowman, A., Buha-Đorđević, A., Paoliello, M. M., Skalny, A.,& Aschner, M.. (2021). Sirtuins as molecular targets, mediators, and protective agents in metal‑induced toxicity. in Archives of Toxicology
Springer..
https://doi.org/10.1007/s00204-021-03048-6

Tinkov A, Nguyen T, Santamaria A, Bowman A, Buha-Đorđević A, Paoliello MM, Skalny A, Aschner M. Sirtuins as molecular targets, mediators, and protective agents in metal‑induced toxicity. in Archives of Toxicology. 2021;.
doi:10.1007/s00204-021-03048-6 .

Tinkov, Alexey, Nguyen, Thuy, Santamaria, Abe, Bowman, Aaron, Buha-Đorđević, Aleksandra, Paoliello, Monica Maria, Skalny, Anatoly, Aschner, Michael, "Sirtuins as molecular targets, mediators, and protective agents in metal‑induced toxicity" in Archives of Toxicology (2021),
https://doi.org/10.1007/s00204-021-03048-6 . .

TY  - JOUR
AU  - Varmazyari, Atefeh
AU  - Taghizadehghalehjoughi, Ali
AU  - Sevim, Cigdem
AU  - Baris, Ozlem
AU  - Eser, Gizem
AU  - Yildirim, Serkan
AU  - Hacimuftuoglu, Ahmet
AU  - Buha, Aleksandra
AU  - Wallace, David R.
AU  - Tsatsakis, Aristidis
AU  - Aschner, Michael
AU  - Mezhuev, Yaroslav
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3593
AB  - Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.
PB  - Elsevier
T2  - Toxicology Reports
T1  - Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies
VL  - 7
SP  - 637
EP  - 648
DO  - 10.1016/j.toxrep.2020.04.011
ER  - 

@article{
author = "Varmazyari, Atefeh and Taghizadehghalehjoughi, Ali and Sevim, Cigdem and Baris, Ozlem and Eser, Gizem and Yildirim, Serkan and Hacimuftuoglu, Ahmet and Buha, Aleksandra and Wallace, David R. and Tsatsakis, Aristidis and Aschner, Michael and Mezhuev, Yaroslav",
year = "2020",
abstract = "Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.",
publisher = "Elsevier",
journal = "Toxicology Reports",
title = "Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies",
volume = "7",
pages = "637-648",
doi = "10.1016/j.toxrep.2020.04.011"
}

Varmazyari, A., Taghizadehghalehjoughi, A., Sevim, C., Baris, O., Eser, G., Yildirim, S., Hacimuftuoglu, A., Buha, A., Wallace, D. R., Tsatsakis, A., Aschner, M.,& Mezhuev, Y.. (2020). Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies. in Toxicology Reports
Elsevier., 7, 637-648.
https://doi.org/10.1016/j.toxrep.2020.04.011

Varmazyari A, Taghizadehghalehjoughi A, Sevim C, Baris O, Eser G, Yildirim S, Hacimuftuoglu A, Buha A, Wallace DR, Tsatsakis A, Aschner M, Mezhuev Y. Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies. in Toxicology Reports. 2020;7:637-648.
doi:10.1016/j.toxrep.2020.04.011 .

Varmazyari, Atefeh, Taghizadehghalehjoughi, Ali, Sevim, Cigdem, Baris, Ozlem, Eser, Gizem, Yildirim, Serkan, Hacimuftuoglu, Ahmet, Buha, Aleksandra, Wallace, David R., Tsatsakis, Aristidis, Aschner, Michael, Mezhuev, Yaroslav, "Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies" in Toxicology Reports, 7 (2020):637-648,
https://doi.org/10.1016/j.toxrep.2020.04.011 . .