Protection of manganese oxide nanoparticles-induced liver and kidney damage by vitamin D

Metal nanoparticles (NPs) have been extensively used in industry as well as in biomedical application. Manganese oxide-nanoparticles (MnO2-NPs) one of these materials, have many applications. This study was designed to evaluate the protective role of vitamin D against MnO2-NPs -induced toxicity in the BALB c mice. These mice were randomly assigned to 4 (n = 10). In this study, MnO2-NPs (10 mg/kg), vitamin D (10 mg/kg) and MnO2-NPs plus vitamin D were administered interperitoneally once daily for 50 consecutive days. The liver and kidney functions, the levels of serum glucose, albumin (ALB), bilirubin (BIL) and total protein were studied. The results indicated that MnO2-NPs administration significantly decreased liver and kidney functions, and increased glucose and bilirubin serum levels compared to control group (P < 0.05). However, vitamin D administration significantly boosted liver and kidney functions, decreased glucose and bilirubin serum level compared to the group received MnO2-NPs (P < 0.05). It seems that vitamin D administration could protect the liver and kidney damage induced by MnO2-NPs. Probably, given the use of these nanoparticles as a contest agent in humans, having normal levels of vitamin D or receiving it at the time of the test can inhibit liver and kidney toxicity induced by MnO2-NPs. © 201

Biocompatibility assessment of titanium dioxide nanoparticles in mice fetoplacental unit

As the applications of titanium dioxide nanomaterials (nTiO2) are growing with an ever-increasing speed, the hazardous risks of this material have become a major concern. Several recent studies have reported that nTiO2 can cross the placental barrier in pregnant mice and cause neurotoxicity in their offspring. However, the influence of these nanoparticles on the fetoplacental unit during the pregnancy is yet to be studied. The present study reports on the effects of nTiO2 on the anatomical structure of fetal brain and liver in a pregnant mice model. Moreover, changes in the size and weight of the fetus and placenta are investigated as markers of fetal growth. Lastly, the toxicity of nTiO2 in primary brain and liver is quantified. Animals treated with nTiO2 showed a disrupted anatomical structure of the fetal brain and liver. Furthermore, the fetus and placental unit in the mice treated with these nanoparticles were smaller compared to untreated controls. Toxicity analyses revealed that nTiO2 was toxic to the brain and liver cells and the mechanism of cell death was mostly necrosis. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 580�589, 2018. © 2017 Wiley Periodicals, Inc

Biocompatibility assessment of titanium dioxide nanoparticles in mice fetoplacental unit

As the applications of titanium dioxide nanomaterials (nTiO2) are growing with an ever-increasing speed, the hazardous risks of this material have become a major concern. Several recent studies have reported that nTiO2 can cross the placental barrier in pregnant mice and cause neurotoxicity in their offspring. However, the influence of these nanoparticles on the fetoplacental unit during the pregnancy is yet to be studied. The present study reports on the effects of nTiO2 on the anatomical structure of fetal brain and liver in a pregnant mice model. Moreover, changes in the size and weight of the fetus and placenta are investigated as markers of fetal growth. Lastly, the toxicity of nTiO2 in primary brain and liver is quantified. Animals treated with nTiO2 showed a disrupted anatomical structure of the fetal brain and liver. Furthermore, the fetus and placental unit in the mice treated with these nanoparticles were smaller compared to untreated controls. Toxicity analyses revealed that nTiO2 was toxic to the brain and liver cells and the mechanism of cell death was mostly necrosis. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 580�589, 2018. © 2017 Wiley Periodicals, Inc

A comparison of mitochondrial toxicity of mephedrone on three separate parts of brain including hippocampus, cortex and cerebellum

Mephedrone (4-methylmethcathinone) is a new and popular drug of abuse and also widely available on the internet and still legal in some parts of the world. The central nervous system is the target of mephedrone and recent evidence suggested that mephedrone could affect mitochondria in brain tissue. However, the underlying mechanisms of mephedrone toxicity in brain mitochondria have not yet been well understood. In this study, mitochondria from three separate parts of rat brain hippocampus, cortex, and cerebellum were obtained using differential centrifugation and were incubated with different concentrations of mephedrone (3, 6 and 12 μM). Then, the mitochondrial parameters toxicity were determined. The results showed that mephedrone (3, 6 and 12 μM) induced impairment in the activity of the mitochondrial complex II and IV. Also, mephedrone (3, 6 and 12 μM) increased mitochondrial reactive oxygen species (ROS) level, collapsed mitochondria membrane potential (MMP), induced swelling in the mitochondria and damaged the mitochondrial outer membrane (MOM) in the mitochondria obtained from hippocampus, cortex, and cerebellum, which in all cases is associated with the cytochrome c release. Furthermore, increased disturbance in oxidative phosphorylation was also shown by the decrease in ATP level in mephedrone-treated mitochondria indicating mitochondrial dysfunction in separate parts of the brain. This study suggests that mephedrone via increasing oxidative stress and impairment of the mitochondrial respiratory chain in the hippocampus, cortex, and cerebellum may play a key role in the neurotoxicity. © 2019 Elsevier B.V

Evaluation of the toxicity effects of silk fibroin on human lymphocytes and monocytes

Silk fibroin nanoparticles (SFNPs) as a natural polymer have been utilized in biomedical applications such as suture, tissue engineering-based scaffolds, and drug delivery carriers. Since there is little data regarding the toxicity effects on different cells and tissues, we aimed to determine the toxicity mechanisms of SFNPs on human lymphocytes and monocytes based on reliable methods. Our results showed that SFNPs (0.5, 1, and 2 mg/mL) induced oxidative stress via increasing reactive oxygen species production, mitochondrial membrane potential ((increment)Ψ) collapse, which was correlated to cytochrome c release and Adenosine diphosphate (ADP)/Adenosine tri phosphate (ATP) ratio increase as well as lysosomal as another toxicity mechanism, which led to cytosolic release of lysosomal digestive proteases, phosphor lipases, and apoptosis signaling. Taken together, these data suggested that SFNPs toxicity was associated with mutual mitochondrial/lysosomal cross-talk and oxidative stress on human lymphocytes and monocytes with activated apoptosis signaling. © 2018 Wiley Periodicals, Inc

Selective toxicity of ag/tio2 nanoparticles of water industrial factories on muscle mitochondria isolated from solendactylus scallop

Industrial wastewater is of global concern due to its severe effects on the environment. Compared with municipal wastewater, industrial wastewater generally contains the high concentration of toxic or no biodegradable pollutants. In recently year, scientific showed that scallop could filtration wastewater. Therefore, it was decided to determine the mechanistic toxicity of wastewater contained NPs (Ag and TiO2) towards isolated mitochondria via reliable methods. Isolated muscle scallop mitochondria were obtained by differential ultracentrifugation on before and after exposure to wastewater. Our results showed that two NPs (Ag and TiO2) induced mitochondrial dysfunction via an increase in mitochondrial reactive oxygen species (ROS) generation, lipid peroxidation (LPO) and mitochondrial membrane potential (MMP) collapse. Finally, Ag-NPs and TiO2NPs have reduced the level of glutathione (GSH) and also induced apoptosis. Our results suggest that wastewater contained NPs-induced toxicity is the result of a disruptive effect on the mitochondrial respiratory chain, increasing the chance of cell death signaling. © 2020, Iranian Association of Pharmaceutical Scientists. All rights reserved

Evaluation of the toxicity effects of silk fibroin on human lymphocytes and monocytes

Silk fibroin nanoparticles (SFNPs) as a natural polymer have been utilized in biomedical applications such as suture, tissue engineering-based scaffolds, and drug delivery carriers. Since there is little data regarding the toxicity effects on different cells and tissues, we aimed to determine the toxicity mechanisms of SFNPs on human lymphocytes and monocytes based on reliable methods. Our results showed that SFNPs (0.5, 1, and 2 mg/mL) induced oxidative stress via increasing reactive oxygen species production, mitochondrial membrane potential (�Ψ) collapse, which was correlated to cytochrome c release and Adenosine diphosphate (ADP)/Adenosine tri phosphate (ATP) ratio increase as well as lysosomal as another toxicity mechanism, which led to cytosolic release of lysosomal digestive proteases, phosphor lipases, and apoptosis signaling. Taken together, these data suggested that SFNPs toxicity was associated with mutual mitochondrial/lysosomal cross-talk and oxidative stress on human lymphocytes and monocytes with activated apoptosis signaling. © 2018 Wiley Periodicals, Inc