Background: Endometriosis is an inflammatory condition featuring persistent
oxidative stress. Usual hormonal therapy and surgery can be limited because they
introduce contraceptive effects. Aim: This review considers the potential of Nacetylcysteine
(NAC) as a candidate non-hormonal molecule that could influence
endometriosis, while considering the preliminary and methodological weaknesses
of the available data. Materials and Methods: A structured PubMed-MEDLINE search
(January 2010 – May 2026) was performed to identify the role of N-acetylcysteine
(NAC) in endometriosis. A comparative approach was used to summarize the
methodological validity of preclinical animal studies and clinical trials and to assess
study quality. Results: Evidence from mechanistic studies and experimental models
indicates NAC as a candidate factor associated with molecular changes in tissue
and lesion regression in preclinical models. Clinical research reports pain relief and
a reduction in endometrioma size; however, the results are affected by small sample
sizes, lack of randomization and placebo control, or mixed antioxidant
formulations. Conclusions: Current knowledge is insufficient to support NAC as a
conventional treatment for endometriosis. Limitations stemming from the heavy
reliance on preclinical models and the confounding design of clinical trials hinder
understanding of NAC’s role. Further research needs to focus on randomized
controlled trials on NAC alone. Showing the disease-modifying potential of NAC
requires long-term outcomes.
Keywords: endometriosis, n-acetylcysteine (NAC), redox signaling modulation,
proliferation-to-differentiation switch
