Acrylamide exposure impairs blood-cerebrospinal fluid barrier function

Area of Science:

• Neuroscience
• Toxicology
• Physiology

Background:

• Chronic acrylamide exposure is known to cause neurotoxicity.
• The precise mechanisms underlying acrylamide-induced neurotoxicity remain incompletely understood.

Purpose of the Study:

• To investigate the effects of acrylamide exposure on the blood-cerebrospinal fluid barrier (BCB) in rats.
• To assess alterations in transthyretin secretion and leptin transport across the BCB following acrylamide exposure.

Main Methods:

• Rats were exposed to acrylamide for 7, 14, 21, or 28 days.
• Blood-cerebrospinal fluid barrier permeability was assessed using sodium fluorescein and Evans blue.
• Transthyretin levels and leptin transport were measured in cerebrospinal fluid.
• Cerebrospinal fluid/serum albumin ratio was analyzed.

Main Results:

• Transthyretin levels in cerebrospinal fluid decreased significantly by day 7.
• Blood-cerebrospinal fluid barrier permeability increased, indicated by elevated sodium fluorescein and Evans blue levels in cerebrospinal fluid from day 14 onwards.
• Leptin transport across the barrier was impaired, shown by a decreased cerebrospinal fluid/serum leptin ratio by days 21 and 28.
• Cerebrospinal fluid/serum albumin ratio increased on day 28.

Conclusions:

• Acrylamide exposure significantly damages the blood-cerebrospinal fluid barrier in a time-dependent manner.
• Impairment of transthyretin secretion and leptin transport across the BCB are key consequences of acrylamide exposure.
• These BCB dysfunctions are likely critical contributors to acrylamide-induced neurotoxicity.