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Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

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Diabetes exacerbates nanoparticles induced brain pathology.

José Vicente Lafuente¹, Aruna Sharma, Ranjana Patnaik

¹Lab Clinical & Experimental Neurosciences (LaCEN), Dept. Neurosciences, University of Basque Country, Box 699, 48080-Bilbao, Spain.

CNS & Neurological Disorders Drug Targets

|January 11, 2012

Summary

Nanoparticle exposure, including silica (SiO2), copper (Cu), and silver (Ag), can worsen neurotoxicity in diabetic individuals. Diabetic animals exhibit greater susceptibility to nanoparticle-induced brain damage compared to healthy ones.

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Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Published on: October 25, 2016

Area of Science:

Environmental toxicology
Neuroscience
Metabolic disease research

Background:

Long-term exposure to nanoparticles (e.g., silica, copper, silver) may impact mental health.
The effects of nanoparticles on individuals with cardiovascular or metabolic diseases, such as hypertension and diabetes, are not well understood.
Diabetic and hypertensive individuals have compromised immune systems, potentially increasing vulnerability to nanoparticle exposure.

Purpose of the Study:

To investigate whether nanoparticles (Cu, Ag, SiO2) exacerbate neurotoxicity in diabetic animal models.
To compare the adverse health effects of nanoparticle exposure in diabetic versus healthy individuals.
To explore the mechanisms underlying enhanced neurotoxicity in diabetic animals exposed to nanoparticles.

Main Methods:

Utilized streptozotocin-induced diabetic rats for experiments.
Administered copper (Cu) or silver (Ag) nanoparticles (50 mg/kg, i.p. per day for 7 days).
Assessed neurotoxicity, sensory, motor, and cognitive functions, blood-brain barrier (BBB) disruption, edema, cell injury, and cerebral blood flow (CBF).

Main Results:

Diabetic rats exposed to Cu or Ag nanoparticles showed enhanced neurotoxicity and functional deficits compared to normal rats.
Diabetic animals exhibited exacerbated blood-brain barrier (BBB) disruption, edema, and cell injuries.
A greater reduction in local cerebral blood flow (CBF) was observed in nanoparticle-exposed diabetic rats.

Conclusions:

Diabetic animals are more vulnerable to nanoparticle-induced brain damage than healthy rats.
Nanoparticle exposure can significantly exacerbate neurotoxicity and neurological deficits in the context of diabetes.
Findings highlight the critical need to consider metabolic health status when assessing risks associated with environmental and industrial nanoparticle exposure.