Table 1 Open in new tab Experimental...

Nanomaterials

Size, nm

Animal model

Exposure route

Dose

Duration

Mechanisms

Major findings

Authors

ZnO NPs

Wistar rats

Intratracheal instillation

1.25, 2.5, 5.0 mg/kg

Once a week, 12 wk

Inflammatory responses; increased HO-1 and PECAM-1

ZnO NPs exposure induced aortic pathological damage.

Yan et al (2017) [13]

CuO NPs

<50

C57BL/6J mice

Intratracheal instillation

5 mg/kg

3 d

Oxidative stress, impaired autophagy

CuO NPs exposure induced vascular endothelial injury

Li et al (2022) [14]

CuO NPs

Zebrafish

Aqueous exposure

0.01, 1, 100 μg/mL

From 1 to 5 dpf

Apoptosis, reduction of expression

CuO NPs exposure inhibited vasculogenesis

Chang et al (2015) [15]

TiO₂NPs

21.6

ApoE-null mice

Intratracheal instillation

0.5 mg/kg

Once a week, 4 wk

No association with inflammation and vasodilatory dysfunction

TiO₂ NPs exposure slightly increased the progression of plaque in the aorta

Mikkelsen et al (2011) [16]

TiO₂NPs

ApoE-null mice

Pharyngeal aspiration

10, 40 μg/mouse

Once a week, 10 wk

Monocyte adhesion; ICAM-1 and F4/80 upregulation

Anatase TiO₂ NPs exposure increased plaque formation in the aorta

Suzuki et al (2020) [17]

MWCNTs

—

ApoE-null mice

Intratracheal instillation

25.6 μg/mouse

Once a week, 5 wk

Oxidative stress, monocyte adhesion; ICAM-1 and VECAM-1 upregulation

MWCNTs exposure accelerated the progression of plaque in the aorta

Cao et al (2014) [18]

MWCNTs

—

Sprague-Dawley rats

Inhalation

5 mg/m³

5 h/d, 7 d

Altered the sympathetic and parasympathetic nervous system

MWCNTs exposure increased both systolic and diastolic blood pressure

Zheng et al (2018) [19]

SWCNTs

—

ApoE-null mice

Pharyngeal aspiration

10, 40 μg/mouse

Once a week, 10 wk

Induction of endothelial progenitor cell dysfunction

SWCNT exposure slightly increased plaque progression in aorta

Suzuki et al (2016) [12]

Table 1

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Experimental studies on the effects on blood vessels of exposure to nanomaterials.

Nanomaterials	Size, nm	Animal model	Exposure route	Dose	Duration	Mechanisms	Major findings	Authors
ZnO NPs	30	Wistar rats	Intratracheal instillation	1.25, 2.5, 5.0 mg/kg	Once a week, 12 wk	Inflammatory responses; increased HO-1 and PECAM-1	ZnO NPs exposure induced aortic pathological damage.	Yan et al (2017) [13]
CuO NPs	<50	C57BL/6J mice	Intratracheal instillation	5 mg/kg	3 d	Oxidative stress, impaired autophagy	CuO NPs exposure induced vascular endothelial injury	Li et al (2022) [14]
CuO NPs	40	Zebrafish	Aqueous exposure	0.01, 1, 100 μg/mL	From 1 to 5 dpf	Apoptosis, reduction of expression	CuO NPs exposure inhibited vasculogenesis	Chang et al (2015) [15]
TiO₂NPs	21.6	ApoE-null mice	Intratracheal instillation	0.5 mg/kg	Once a week, 4 wk	No association with inflammation and vasodilatory dysfunction	TiO₂ NPs exposure slightly increased the progression of plaque in the aorta	Mikkelsen et al (2011) [16]
TiO₂NPs	20	ApoE-null mice	Pharyngeal aspiration	10, 40 μg/mouse	Once a week, 10 wk	Monocyte adhesion; ICAM-1 and F4/80 upregulation	Anatase TiO₂ NPs exposure increased plaque formation in the aorta	Suzuki et al (2020) [17]
MWCNTs	—	ApoE-null mice	Intratracheal instillation	25.6 μg/mouse	Once a week, 5 wk	Oxidative stress, monocyte adhesion; ICAM-1 and VECAM-1 upregulation	MWCNTs exposure accelerated the progression of plaque in the aorta	Cao et al (2014) [18]
MWCNTs	—	Sprague-Dawley rats	Inhalation	5 mg/m³	5 h/d, 7 d	Altered the sympathetic and parasympathetic nervous system	MWCNTs exposure increased both systolic and diastolic blood pressure	Zheng et al (2018) [19]
SWCNTs	—	ApoE-null mice	Pharyngeal aspiration	10, 40 μg/mouse	Once a week, 10 wk	Induction of endothelial progenitor cell dysfunction	SWCNT exposure slightly increased plaque progression in aorta	Suzuki et al (2016) [12]

Nanomaterials	Size, nm	Animal model	Exposure route	Dose	Duration	Mechanisms	Major findings	Authors
ZnO NPs	30	Wistar rats	Intratracheal instillation	1.25, 2.5, 5.0 mg/kg	Once a week, 12 wk	Inflammatory responses; increased HO-1 and PECAM-1	ZnO NPs exposure induced aortic pathological damage.	Yan et al (2017) [13]
CuO NPs	<50	C57BL/6J mice	Intratracheal instillation	5 mg/kg	3 d	Oxidative stress, impaired autophagy	CuO NPs exposure induced vascular endothelial injury	Li et al (2022) [14]
CuO NPs	40	Zebrafish	Aqueous exposure	0.01, 1, 100 μg/mL	From 1 to 5 dpf	Apoptosis, reduction of expression	CuO NPs exposure inhibited vasculogenesis	Chang et al (2015) [15]
TiO₂NPs	21.6	ApoE-null mice	Intratracheal instillation	0.5 mg/kg	Once a week, 4 wk	No association with inflammation and vasodilatory dysfunction	TiO₂ NPs exposure slightly increased the progression of plaque in the aorta	Mikkelsen et al (2011) [16]
TiO₂NPs	20	ApoE-null mice	Pharyngeal aspiration	10, 40 μg/mouse	Once a week, 10 wk	Monocyte adhesion; ICAM-1 and F4/80 upregulation	Anatase TiO₂ NPs exposure increased plaque formation in the aorta	Suzuki et al (2020) [17]
MWCNTs	—	ApoE-null mice	Intratracheal instillation	25.6 μg/mouse	Once a week, 5 wk	Oxidative stress, monocyte adhesion; ICAM-1 and VECAM-1 upregulation	MWCNTs exposure accelerated the progression of plaque in the aorta	Cao et al (2014) [18]
MWCNTs	—	Sprague-Dawley rats	Inhalation	5 mg/m³	5 h/d, 7 d	Altered the sympathetic and parasympathetic nervous system	MWCNTs exposure increased both systolic and diastolic blood pressure	Zheng et al (2018) [19]
SWCNTs	—	ApoE-null mice	Pharyngeal aspiration	10, 40 μg/mouse	Once a week, 10 wk	Induction of endothelial progenitor cell dysfunction	SWCNT exposure slightly increased plaque progression in aorta	Suzuki et al (2016) [12]

Abbreviations: ApoE, apolipoprotein E; dpf, days post-fertilization; HO-1, heme oxygenase-1; ICAM-1, intercellular adhesion molecule-1; MWCNT, multi-walled carbon nanotube; NP, nanoparticle; PECAM-1, platelet endothelial cell adhesion molecule-1; SWCNT, single-walled carbon nanotube; VECAM-1, vascular cell adhesion protein-1; VEGF, vascular endothelial growth factor.

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