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SiO₂ nanoparticle-induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a Kupffer cell-mediated pathway in vitro.

Xue Y, Chen Q, Ding T, Sun J - Int J Nanomedicine (2014)

Bottom Line: First, a buffalo rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiratory chain complexes I, III and IV.The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells.We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiratory chain complex I activity in BRL cells.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Biomaterials Research and Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.

ABSTRACT
The liver has been shown to be a primary target organ for SiO2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a buffalo rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiratory chain complexes I, III and IV. Second, the role of rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiratory chain complex I activity in BRL cells.

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Transmission electron microscopic images of BRL cells treated with SiO2 nanoparticles (1 mg/mL) for 1 hour.Notes: (A) Image of the whole cell. (B) Image of the gated part of (A). Nanoparticles are indicated with white arrows, the particle-filled vesicle is indicated with a black arrow, and the damaged mitochondria are indicated with arrow heads. (C) Image of SiO2 nanoparticles close up in vesicles. The bars represent 2 μm (A) and 1 μm (B and C).Abbreviation: BRL, buffalo rat liver.
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f3-ijn-9-2891: Transmission electron microscopic images of BRL cells treated with SiO2 nanoparticles (1 mg/mL) for 1 hour.Notes: (A) Image of the whole cell. (B) Image of the gated part of (A). Nanoparticles are indicated with white arrows, the particle-filled vesicle is indicated with a black arrow, and the damaged mitochondria are indicated with arrow heads. (C) Image of SiO2 nanoparticles close up in vesicles. The bars represent 2 μm (A) and 1 μm (B and C).Abbreviation: BRL, buffalo rat liver.

Mentions: The morphology of BRL cells following exposure to 1 mg/mL of SiO2 nanoparticles for one hour was examined by TEM. As shown in Figure 3A–C, small particle aggregates were visible. Some small particle aggregates were localized in the cytoplasmic vesicles of the cell, while some aggregates were free in the cytoplasm. Notably, swelling mitochondria with vacuolization and reduced crests were found near the particles that were free in the cytoplasm (Figure 3B).


SiO₂ nanoparticle-induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a Kupffer cell-mediated pathway in vitro.

Xue Y, Chen Q, Ding T, Sun J - Int J Nanomedicine (2014)

Transmission electron microscopic images of BRL cells treated with SiO2 nanoparticles (1 mg/mL) for 1 hour.Notes: (A) Image of the whole cell. (B) Image of the gated part of (A). Nanoparticles are indicated with white arrows, the particle-filled vesicle is indicated with a black arrow, and the damaged mitochondria are indicated with arrow heads. (C) Image of SiO2 nanoparticles close up in vesicles. The bars represent 2 μm (A) and 1 μm (B and C).Abbreviation: BRL, buffalo rat liver.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061170&req=5

f3-ijn-9-2891: Transmission electron microscopic images of BRL cells treated with SiO2 nanoparticles (1 mg/mL) for 1 hour.Notes: (A) Image of the whole cell. (B) Image of the gated part of (A). Nanoparticles are indicated with white arrows, the particle-filled vesicle is indicated with a black arrow, and the damaged mitochondria are indicated with arrow heads. (C) Image of SiO2 nanoparticles close up in vesicles. The bars represent 2 μm (A) and 1 μm (B and C).Abbreviation: BRL, buffalo rat liver.
Mentions: The morphology of BRL cells following exposure to 1 mg/mL of SiO2 nanoparticles for one hour was examined by TEM. As shown in Figure 3A–C, small particle aggregates were visible. Some small particle aggregates were localized in the cytoplasmic vesicles of the cell, while some aggregates were free in the cytoplasm. Notably, swelling mitochondria with vacuolization and reduced crests were found near the particles that were free in the cytoplasm (Figure 3B).

Bottom Line: First, a buffalo rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiratory chain complexes I, III and IV.The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells.We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiratory chain complex I activity in BRL cells.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Biomaterials Research and Testing Center, Shanghai Key Laboratory of Stomatology, Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.

ABSTRACT
The liver has been shown to be a primary target organ for SiO2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a buffalo rat liver (BRL) cell line was directly exposed to SiO2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiratory chain complexes I, III and IV. Second, the role of rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiratory chain complex I activity in BRL cells.

Show MeSH
Related in: MedlinePlus