Fluoride-induced renal dysfunction via respiratory chain complex abnormal expression and fusion elevation in mice

Area of Science:

• Toxicology
• Mitochondrial Biology
• Renal Physiology

Background:

• Fluoride is a common environmental element with known health effects.
• Mitochondrial dysfunction is implicated in various organ damages.
• The specific impact of fluoride on mitochondrial respiratory chain complexes and renal function requires further elucidation.

Purpose of the Study:

• To investigate the effects of excessive fluoride exposure on renal structure and function in a mouse model.
• To examine the relationship between fluoride-induced renal dysfunction and the expression of mitochondrial fusion proteins and respiratory chain complexes.

Main Methods:

• Establishment of a fluoride exposure mouse model.
• Assessment of kidney tissue morphology, renal function, and cell proliferation.
• Quantification of mitochondrial fusion proteins (Mfn1, OPA1) and respiratory chain complex subunits (NDUFV2, SDHA, CYC1, COX IV) using RT-PCR, immunohistochemistry, and Western blot.

Main Results:

• Excessive fluoride exposure caused significant damage to renal tubule, glomerulus, and papilla structures.
• Renal function was impaired, and renal cell proliferation was inhibited.
• Increased expression of Mfn1, OPA1, NDUFV2, CYC1, and COX IV, with decreased SDHA expression at both mRNA and protein levels.

Conclusions:

• Excessive fluoride exposure induces kidney damage and inhibits renal cell proliferation.
• Fluoride exposure disrupts the expression of mitochondrial respiratory chain complexes and promotes mitochondrial fusion.
• These alterations contribute to the development of renal dysfunction.