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Published on: October 29, 2019
Learning and memory impairment of mice caused by gaseous formaldehyde
Fuhong Li1, Yujie Qin1, Siying Gong1
1Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, Hubei, China.
Abstract:
In order to study the e of formaldehyde exposure on learning and memory ability of mice. We used Kun Ming (KM) mice to demonstrate the neurotoxic effects of FA, and Balb/c mice to explore the neurobiological mechanism. The Morris water maze (MWM) test showed that the exposure of gaseous formaldehyde could cause spatial learning and memory impairment in mice. H & E staining showed that in the 3.0 mg/m3 formaldehyde exposed group, the arrangement of pyramidal cells in CA1 area of mouse hippocampus was loose and disordered, the cell morphology was swollen and deformed, and the apical dendrites were shortened or even disappeared. Biochemical indicators revealed high doses of FA exposure could cause oxidative damage in brain. Compared with the control group, there were significant differences in the levels of ROS, MDA, GSH and 8-OHDG in the 3.0 mg/m3 group (P < 0.01), also the monoamine neurotransmitters content and the content of TNF-α, IL-1β and Caspase-3 (P < 0.01). Furthermore, the concentrations of cAMP, cGMP, NO and the activity of NOS in the cerebral cortex, hippocampus and brain stem after high doses of FA exposure were significantly different from those in the control group, indicating that FA exposure could interfere with the transduction of NO/cGMP signaling pathway. The results showed that FA could induce cognitive deficits and this extended investigation found that the toxicity of FA to the mouse nervous system is related to the NO/cGMP and cAMP signaling pathways.
Insights
Formaldehyde exposure impairs learning and memory in mice, causing neuroinflammation and oxidative stress. This toxicity is linked to disruptions in the nitric oxide/cyclic guanosine monophosphate and cyclic adenosine monophosphate signaling pathways.
Area of Science:
- Neuroscience
- Toxicology
- Environmental Health
Background:
- Formaldehyde (FA) is a common environmental pollutant with known toxic effects.
- Understanding its impact on cognitive function and underlying neurobiological mechanisms is crucial.
Purpose of the Study:
- To investigate the effects of formaldehyde exposure on learning and memory in mice.
- To elucidate the neurobiological mechanisms of formaldehyde-induced neurotoxicity.
Main Methods:
- Utilized Kun Ming (KM) and Balb/c mice for behavioral and mechanistic studies.
- Employed the Morris water maze (MWM) test for spatial learning and memory assessment.
- Conducted histological (H&E staining) and biochemical analyses (oxidative stress markers, neurotransmitters, inflammatory cytokines, signaling molecules).
Main Results:
- Formaldehyde exposure significantly impaired spatial learning and memory in mice.
- Histological examination revealed neuronal damage in the hippocampus (CA1 area) of exposed mice.
- Biochemical analyses indicated increased oxidative stress (ROS, MDA, 8-OHDG), altered neurotransmitter levels, and elevated inflammatory markers (TNF-α, IL-1β, Caspase-3).
- Formaldehyde exposure interfered with the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) and cyclic adenosine monophosphate (cAMP) signaling pathways.
Conclusions:
- Formaldehyde exposure induces cognitive deficits in mice.
- The neurotoxicity of formaldehyde is associated with oxidative damage, neuroinflammation, and dysregulation of NO/cGMP and cAMP signaling pathways.

