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Updated: Aug 22, 2026

Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
Published on: September 16, 2020
Mitochondrial dysfunction: patient monitoring and toxicity management
Grace McComsey1, J Tyler Lonergan
1Case Western Reserve University, Cleveland, OH 44106 , USA. mccomsey.grace@clevelandactu.org
Abstract:
Mitochondrial toxicity has been implicated in the development of a variety of nucleoside reverse transcriptase inhibitor-associated syndromes. Mitochondrial damage and decreases in mitochondrial DNA levels have been demonstrated in various tissues of patients treated with NRTIs, especially in conjunction with exposure to stavudine. Clinical syndromes that may be mediated by mitochondrial toxicity include hyperlactatemia and lactic acidosis, hepatic steatosis, lipoatrophy, peripheral neuropathy, HIV-associated neuromuscular weakness syndrome, pancreatitis, skeletal myopathies, and cardiomyopathy. Early recognition of these syndromes in their mild forms involves close monitoring and a high index of suspicion. This may allow prompt discontinuation of the causative agent(s) and initiation of appropriate therapeutic measures, thereby increasing the chances of reversibility of the syndrome.
Insights
Nucleoside reverse transcriptase inhibitors (NRTIs) can cause mitochondrial toxicity, leading to serious health issues. Early detection and stopping NRTIs can help reverse these toxic effects.
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Mitochondrial toxicity is linked to nucleoside reverse transcriptase inhibitor (NRTI) use.
- NRTI treatment, particularly with stavudine, can cause mitochondrial DNA depletion and damage.
Purpose of the Study:
- To review the clinical syndromes associated with NRTI-induced mitochondrial toxicity.
- To emphasize the importance of early recognition and intervention for NRTI-associated mitochondrial syndromes.
Main Methods:
- Literature review of NRTI-associated mitochondrial toxicity.
- Analysis of clinical manifestations and diagnostic considerations.
Main Results:
- Mitochondrial toxicity manifests as hyperlactatemia, lactic acidosis, hepatic steatosis, lipoatrophy, neuropathy, myopathy, and cardiomyopathy.
- Stavudine is frequently implicated in NRTI-associated mitochondrial damage.
Conclusions:
- Early identification of NRTI-induced mitochondrial syndromes is crucial.
- Prompt discontinuation of causative NRTIs can lead to syndrome reversibility.
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