What Does Antioxidant Mean? Are Antioxidant Foods Always Protective?

Chemical reactions involving oxygen used to convert food into energy produce oxygen radicals. These unstable molecules cause oxidative stress. Seeking stability, they attack other molecules and even damage DNA. Cells sensing this stress consequently direct themselves toward death (apoptosis, programmed cell death). An article published in the respected journal Cell on 11 August observed that antioxidant use caused pancreatic cancer progression, meaning worsening disease.

Because cells need energy and energy production requires oxygen, formation of oxygen radicals is natural and inevitable. They can be considered raw-material waste, with antioxidants recycling it. Protection comes from substances produced by the body, such as glutathione peroxidase and superoxide dismutase enzymes, and externally obtained antioxidants . These protect against oxidative stress, but in cancer patients may make treatment harder.

The study examined how mutated (genetically altered) KRAS protein affects an intracellular signaling mechanism, NRF2 , and how this affects the pancreas. KRAS normally transmits proliferation signals. Mutation causes continuous proliferation signaling. Cancers where this is best characterized are colorectal, pancreatic and lung cancers.

Pancreatic cancershows mutations in KRAS and tumor suppressor genes in %95 of cases. Mutated KRAS also increases activity in oxidative balance-regulating pathways, particularly NRF2.

Cell division requires much energy, whose production generates many oxygen radicals, a type of waste. Rapidly dividing cancer cells therefore produce large amounts. Increased oxidative stress and KRAS mutation accelerate NRF2 activity.

The NRF2 pathway increases antioxidant response gene activity to reduce oxidative stress. One NRF2 effect is activating glutathione synthesis. Glutathione is among the body's most important antioxidants, reacting with radicals to stabilize them. It also supports DNA repair and stimulates enzyme synthesis in the pentose phosphate pathway, supporting cancer cells' normal metabolism.

When NRF2 was disabled, oxygen radicals increased, mRNA formation, a protein synthesis step, was disrupted, and cell division-stimulating signaling (EGFR) was impaired. Cell division consequently slowed.

These observations suggest: Increasing oxidative stress in cancer cells may cause cell death. Antioxidants reducing oxidative stress may therefore be harmful.

In conclusion, antioxidantsprotect healthy cells from oxidative stress and DNA damage, allowing healthy cell cycles and division. But this same beneficial property can support cancer cell division, disease progression and reduced treatment response. Slowing the antioxidant NRF2 pathway disrupted normal cellular function and directed cells toward death, offering hope of improved treatment success. We should therefore use medicines and herbal products containing vitamins and antioxidants only with our doctors' knowledge.