Buffering Mitigates Chondrocyte Oxidative Stress, Metabolic Dysfunction, and Death Induced by Normal Saline: Formulation of a Novel Arthroscopic Irrigant

Arman Hlas; Venkateswaran Ganesh; Jaison Marks; Rui He; Aliasger K Salem; Joseph A Buckwalter; Kyle R Duchman; Kyungsup Shin; James A Martin; Dongrim Seol

doi:10.3390/ijms25021286

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Buffering Mitigates Chondrocyte Oxidative Stress, Metabolic Dysfunction, and Death Induced by Normal Saline: Formulation of a Novel Arthroscopic Irrigant

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Buffering Mitigates Chondrocyte Oxidative Stress, Metabolic Dysfunction, and Death Induced by Normal Saline: Formulation of a Novel Arthroscopic Irrigant

Arman Hlas, Venkateswaran Ganesh, Jaison Marks, Rui He, Aliasger K Salem, Joseph A Buckwalter, Kyle R Duchman, Kyungsup Shin, James A Martin and Dongrim Seol

International journal of molecular sciences, Vol.25(2), 1286

01/20/2024

DOI: 10.3390/ijms25021286

PMCID: PMC10816598

PMID: 38279286

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Abstract

For decades, surgeons have utilized 0.9% normal saline (NS) for joint irrigation to improve visualization during arthroscopic procedures. This continues despite mounting evidence that NS exposure impairs chondrocyte metabolism and compromises articular cartilage function. We hypothesized that chondrocyte oxidative stress induced by low pH is the dominant factor driving NS toxicity, and that buffering NS to increase its pH would mitigate these effects. Effects on chondrocyte viability, reactive oxygen species (ROS) production, and overall metabolic function were assessed. Even brief exposure to NS caused cell death, ROS overproduction, and disruption of glycolysis, pentose phosphate, and tricarboxylic acid (TCA) cycle pathways. NS also stimulated ROS overproduction in synovial cells that could adversely alter the synovial function and subsequently the entire joint health. Buffering NS with 25 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) significantly increased chondrocyte viability, reduced ROS production, and returned metabolite levels to near control levels while also reducing ROS production in synovial cells. These results confirm that chondrocytes and synoviocytes are vulnerable to insult from the acidic pH of NS and demonstrate that adding a buffering agent to NS averts many of its most harmful effects.

Oxidative Stress

normal saline

acidity

chondrocyte

cell death

HEPES

metabolic dysfunction

reactive oxygen species

synoviocyte

arthroscopic irrigation

Details

Title: Subtitle: Buffering Mitigates Chondrocyte Oxidative Stress, Metabolic Dysfunction, and Death Induced by Normal Saline: Formulation of a Novel Arthroscopic Irrigant
Creators: Arman Hlas - University of Iowa
Venkateswaran Ganesh - University of Iowa
Jaison Marks - Roy J. Carver Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA
Rui He - University of Iowa
Aliasger K Salem - University of Iowa
Joseph A Buckwalter - University of Iowa
Kyle R Duchman - University of Iowa
Kyungsup Shin - Department of Orthodontics, College of Dentistry and Dental Clinics, University of Iowa, Iowa City, IA 52242, USA
James A Martin - University of Iowa
Dongrim Seol - University of Iowa
Resource Type: Journal article
Publication Details: International journal of molecular sciences, Vol.25(2), 1286
DOI: 10.3390/ijms25021286
PMID: 38279286
PMCID: PMC10816598
NLM abbreviation: Int J Mol Sci
ISSN: 1422-0067
eISSN: 1422-0067
Grant note: No grant number / the Carver College of Medicine Summer Research Fellowship and the Department of Orthopedics and Rehabilitation at the University of Iowa
Language: English
Date published: 01/20/2024
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Orthodontics; Pharmaceutical Sciences and Experimental Therapeutics; Orthopedics and Rehabilitation; Craniofacial Anomalies Research Center; Injury Prevention Research Center; Dental Research; Chemical and Biochemical Engineering
Record Identifier: 9984548465902771

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