How MitoQ Mitoquinol may help protect us from microplastics

Microplastics are an emerging concern, and research in animals shows that antioxidants like MitoQ® Mitoquinol might offer a way to address the effects of microplastics. A new study sheds light on how polystyrene microplastics (which come from things like polystyrene cups and packing materials), can cause neurotoxic effects in animals. In the study, these microplastics were found to create oxidative stress and damage neurons. The intriguing result? A specialized antioxidant, MitoQ® Mitoquinol, showed to be a powerful protector of mitochondrial health, counteracting the effects of these microplastics.

What Did the Study Reveal?

Overall, MitoQ® Mitoquinol was shown to help to protect against some of the toxic effects of microplastics in a few ways:

Lowering Harmful Free Radicals (ROS):
Exposure to polystyrene microplastics triggered the production of reactive oxygen species (ROS)—unstable molecules that cause oxidative stress. MitoQ® Mitoquinol effectively reduced ROS levels, helping to curb the damage.

Supporting Natural Defences:
The study showed that MitoQ® Mitoquinol boosted the regulation of an enzyme called Sod-2, a key player in defending cells from oxidative stress. By enhancing Sod-2 expression, MitoQ® Mitoquinol added another layer of protection against nanoplastic-induced damage.

Protecting Nerve Health and Behaviour:
Through its dual action—reducing ROS and increasing Sod-2— MitoQ® Mitoquinol mitigated potential harm to neurons.

Why Does This Matter?

Environmental pollutants like microplastics can remain in the ecosystem and bio accumulate up the food chain to eventually be consumed by us. This is likely to pose a threat to human health as polystyrene microplastics are known to be toxic. In animal models, these microplastics have shown to disrupt female reproductive health, impact male infertility, impair memory, and can affect the lungs when inhaled.

These recent findings highlight MitoQ® Mitoquinol's potential in guarding against neurotoxicity caused by microplastics. While this research is based on an animal model, the implications may extend to other animals and human health.

This study is a stepping stone toward better understanding how mitochondria-targeted therapies could help protect against environmental toxins. Further research will help uncover how we might harness these insights to promote healthier, more resilient cells in the face of modern environmental challenges.