Sodium fluoride induces apoptosis in the kidney of rats through caspase-mediated pathways and DNA damage

Related Experiment Video

Updated: Apr 25, 2026

Micro-dissection of Enamel Organ from Mandibular Incisor of Rats Exposed to Environmental Toxicants
08:12

Micro-dissection of Enamel Organ from Mandibular Incisor of Rats Exposed to Environmental Toxicants

Published on: March 29, 2018

9.8K

Guo Hua Song1, Ji Ping Gao, Chun Fang Wang

  • 1Laboratory Animal Center, Shanxi Medical University, Road Xinjian 56, Taiyuan, 030001, China, ghsongg@hotmail.com.

Journal of Physiology and Biochemistry
|August 28, 2014
PubMed

Insights

Excessive sodium fluoride (NaF) intake damages kidney cells by increasing apoptosis and DNA damage. This occurs via a caspase-mediated pathway involving cytochrome C release.

Area of Science:

  • Toxicology
  • Renal Physiology
  • Cellular Biology

Background:

  • Long-term excessive sodium fluoride (NaF) intake is linked to bone diseases and nonskeletal fluorosis.
  • The kidneys play a crucial role in the excretion and retention of NaF.
  • Understanding NaF's renal effects is vital for public health.

Purpose of the Study:

  • To investigate the impact of NaF on renal cell apoptosis and DNA damage in vivo.
  • To examine the protein expression of key apoptosis-related factors, including cytosolic cytochrome C (Cyt C) and caspases 9, 8, and 3, following NaF exposure.
  • To elucidate the molecular mechanisms underlying NaF-induced kidney injury.

Main Methods:

  • Male Sprague-Dawley rats were exposed to varying concentrations of NaF (0, 50, 100, 200 mg/L) in drinking water for 120 days.
  • Kidney histopathology was assessed using hematoxylin and eosin staining.
  • Renal cell apoptosis was quantified by flow cytometry, and DNA damage was evaluated using the comet assay.
  • Protein expression of Cyt C and cleaved caspases was determined via immunohistochemistry and Western blotting.

Main Results:

  • NaF treatment led to a dose-dependent increase in renal cell apoptosis and DNA damage.
  • Elevated levels of cytosolic Cyt C and cleaved caspases 9, 8, and 3 were observed in NaF-exposed kidneys.
  • Histopathological examination revealed kidney tissue alterations consistent with cellular injury.

Conclusions:

  • Sodium fluoride induces apoptosis in rat kidneys through a caspase-mediated pathway.
  • DNA damage is implicated as a contributing factor in NaF-induced renal apoptosis.
  • These findings highlight the nephrotoxic potential of excessive NaF exposure.

More Related Videos

High Throughput SiRNA Screening for Chloropicrin and Hydrogen Fluoride-Induced Cornea Epithelial Cell Injury14:20

High Throughput SiRNA Screening for Chloropicrin and Hydrogen Fluoride-Induced Cornea Epithelial Cell Injury

Published on: June 16, 2018

6.0K
Flow Cytometric Analysis of Apoptotic Biomarkers in Actinomycin D-Treated SiHa Cervical Cancer Cells13:53

Flow Cytometric Analysis of Apoptotic Biomarkers in Actinomycin D-Treated SiHa Cervical Cancer Cells

Published on: August 26, 2021

6.8K

Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.9K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.1K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
8.6K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.2K
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
71