Light Therapy Boosts Lifespan and Stress Resistance in Tiny Worms

Jim Crocker
17th May, 2024

Light Therapy Boosts Lifespan and Stress Resistance in Tiny Worms

Image Source: Natural Science News, 2024

Key Findings

  • The study by the Korea Institute of Science and Technology (KIST) used a novel photodynamic treatment (PDTr) with hypericin and orange light to induce mild ROS formation in C. elegans
  • This treatment extended the lifespan and improved stress resistance in C. elegans by activating transcription factors SKN-1/NRF-2 and DAF-16/FOXO, which increased the expression of antioxidant genes
  • The lifespan extension was driven by prooxidative mechanisms, as evidenced by the fact that it was negated by the antioxidant N-acetyl cysteine
Reactive oxygen species (ROS) are highly reactive molecules that play a dual role in cellular health. While high levels of ROS can cause oxidative damage and contribute to aging and diseases, moderate levels are essential for various cellular functions, including gene expression and programmed cell death[2]. This paradoxical nature of ROS has led scientists to explore their potential therapeutic applications, particularly in cancer treatment and lifespan extension. A recent study conducted by the Korea Institute of Science and Technology (KIST) has introduced a novel photodynamic treatment (PDTr) using 20 μM hypericin, a photosensitizer derived from Hypericum perforatum, and orange light (590 nm, 5.4 W/m², 1 min) to induce mild ROS formation. This study found that such a treatment could extend the lifespan and improve stress resistance in the model organism C. elegans[1]. Photodynamic therapy (PDT) is a noninvasive treatment that uses specific photosensitizers and light to produce high amounts of ROS, traditionally employed for targeted tissue destruction in cancer treatment and antimicrobial therapy. However, the KIST study aimed to investigate whether lower amounts of ROS produced by mild photodynamic therapy could have beneficial effects at the organism level, particularly in terms of lifespan extension and stress resistance. The study demonstrated that PDTr activated the translocation of SKN-1/NRF-2 and DAF-16/FOXO, transcription factors known to regulate oxidative stress response genes. This activation led to the elevated expression of antioxidant genes such as ctl-1, gst-4, and sod-3. The increased lifespan and stress resistance observed in C. elegans were found to be mediated by these oxidative stress-responsive genes. The concept of using ROS to extend lifespan is supported by earlier studies. For instance, the theory of mitochondrial hormesis (mitohormesis) suggests that low levels of ROS can improve systemic defense mechanisms by inducing an adaptive response, ultimately extending lifespan[3]. Another study showed that in Saccharomyces cerevisiae, caloric restriction or inactivation of catalases extended lifespan by inducing elevated levels of hydrogen peroxide, which activated superoxide dismutases to inhibit the accumulation of superoxide anions[4]. These findings align with the KIST study, which also observed lifespan extension through prooxidative mechanisms. Interestingly, the KIST study found that the lifespan extension induced by PDTr was abrogated by N-acetyl cysteine, an antioxidant. This suggests that the hormetic response was driven by prooxidative mechanisms rather than antioxidant effects. This finding is consistent with other research indicating that antioxidants might interfere with beneficial ROS signals and could even be harmful[3]. Moreover, the KIST study contributes to the growing body of evidence that environmental stresses experienced during development can have long-term health benefits. For example, a study in Drosophila showed that transient exposure to low concentrations of oxidants during development extended adult lifespan by selectively depleting harmful bacteria in the microbiome, rather than through mitohormesis[5]. While the mechanisms differ, both studies highlight the potential for low-dose oxidative stress to confer long-term benefits. In summary, the KIST study introduces a novel photodynamic treatment that uses mild ROS formation to extend lifespan and improve stress resistance in C. elegans. This treatment activates key transcription factors and oxidative stress-responsive genes, suggesting a prooxidative mechanism behind the observed benefits. These findings align with and expand upon previous research, highlighting the complex and beneficial roles of ROS in cellular health and longevity.



Main Study

1) Photodynamic treatment increases the lifespan and oxidative stress resistance of Caenorhabditis elegans.

Published 14th May, 2024

Related Studies

2) ROS in cancer therapy: the bright side of the moon.

3) Mitohormesis: Promoting Health and Lifespan by Increased Levels of Reactive Oxygen Species (ROS).

4) Caloric restriction or catalase inactivation extends yeast chronological lifespan by inducing H2O2 and superoxide dismutase activity.

5) Early-life exposure to low-dose oxidants can increase longevity via microbiome remodelling in Drosophila.

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