MTA does not induce oxidative stress and apoptotic response, or calcium-related cellular stress and preserves

Okan Sancer1, Deniz Yanık Nalbantoğlu2, Ahmet Mert Nalbantoğlu3

  • 1Genetic Research Unit, Innovative Technologies Application and Research Center, Süleyman Demirel University, Isparta, Turkey.

Abstract

Insights

Mineral Trioxide Aggregate (MTA) maintained cell viability and molecular balance in fibroblasts over time. MTA did not trigger oxidative stress, apoptosis, or calcium imbalance, indicating good biocompatibility.

Area of Science:

  • Biomaterials Science
  • Cell Biology
  • Molecular Biology

Background:

  • Mineral Trioxide Aggregate (MTA) is widely used in dentistry.
  • Understanding its early biological effects is crucial for clinical application.
  • Investigating time-dependent cellular responses to MTA is essential.

Purpose of the Study:

  • To evaluate the time-dependent biological effects of MTA on L-929 fibroblasts.
  • To assess MTA's impact on cellular viability and gene expression.
  • To analyze gene expression related to oxidative stress, apoptosis, calcium homeostasis, and extracellular matrix.

Main Methods:

  • L-929 fibroblasts were exposed to MTA eluates at different time points (4, 6, 8, 24 hours).
  • Cell viability was measured using the MTT assay.
  • Gene expression levels of Nrf2, p53, CALB1, and FN were analyzed via real-time PCR.

Main Results:

  • Cell viability remained above the 70% biocompatibility threshold across all tested time points.
  • A statistically significant fluctuation in cell viability was observed between 4h and 6h, and 4h and 8h.
  • No significant differences in Nrf2, p53, CALB1, or FN gene expression were found between MTA-treated and control groups.

Conclusions:

  • MTA demonstrates biocompatibility by preserving cellular viability and molecular homeostasis.
  • MTA does not induce oxidative stress, apoptosis, or calcium imbalance during its setting phase.
  • Stable gene expression suggests MTA's ability to maintain intracellular equilibrium contributes to its favorable clinical performance.

Related Concept Videos

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...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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...