Lactose induced redox-dependent senescence and activated Nrf2 pathway

Area of Science:

• Cell Biology
• Aging Research
• Biochemistry

Background:

• Lactose is a milk disaccharide, normally digested by lactase.
• Lactose intolerance results from lactase deficiency, causing digestive issues.
• The impact of lactose on cellular senescence is largely unknown.

Purpose of the Study:

• To investigate the effects of lactose on cellular senescence.
• To elucidate the underlying mechanisms of lactose-induced senescence.
• To assess the potential of antioxidants to mitigate these effects.

Main Methods:

• Cellular senescence markers (SA-β-gal, p16^ink4a) were measured in MRC-5 cells.
• Cell viability was assessed using the CCK-8 Assay.
• Oxidative stress markers (ROS, SOD, GSH) and the Nrf2/ARE pathway were analyzed.
• Lifespan studies were conducted in *Caenorhabditis elegans*.
• The effect of N-Acetyl-L-cysteine (NAC) was evaluated.

Main Results:

• Lactose increased SA-β-gal and p16^ink4a expression, indicating induced senescence.
• Lactose elevated ROS and decreased SOD and GSH levels, signifying oxidative stress.
• The Nrf2/ARE pathway was implicated in lactose-induced oxidative stress.
• Lactose supplementation shortened the lifespan of *C. elegans*.
• NAC treatment alleviated lactose-induced senescence and oxidative stress.

Conclusions:

• Lactose induces cellular senescence, potentially through oxidative stress.
• The Nrf2/ARE pathway plays a role in lactose-mediated oxidative stress.
• Antioxidant intervention, such as with NAC, can counteract lactose-induced senescence.