Antioxidant Detoxification Is Crucial For Effective Acne Treatment

Acne vulgaris is a usual skin disease of adolescence. Its pathogenesis is associated with a number of factors, including disturbed cornification within the pilosebaceous unit and increased microbial colonization of the whole sebum ducts.

Propionibacterium acnes (P. acnes), an anaerobic organism, multiplies in the mix of sebum and follicular cells, leading to the production of inflammatory compounds with neutrophil chemotaxis. In addition, P. acnes elaborates various degradative enzymes which could be involved in destruction of the follicular wall and lead to the exacerbation of inflammation. However, while neutrophils produce reactive oxygen species (ROS) for eliminating the microorganisms, excessive generation of ROS may enhance the destruction of surrounding healthy tissues and lead to demeaning acne scars.

exacerbation of inflammation

The most essential process in acne inflammation is considered to be the damage to the follicular epithelium. It has been reported that ROS generated by neutrophils within the follicular wall cause tissue injury at the swelling site. ROS are responsible for the irritation and destruction of the follicular wall that ends with swelling and development of acne.

But also the hardenning of sebum due to a depletion of linoleic acid in the sebum glands brough forth by high production of sebum. Hard sebum injures the cells lining the follicular walls by punctures and cuts and abrasions. Akamatsu et al.  discovered decreased linoleic acid levels in comedonal acne; this acid prevents neutrophil ROS generation.

GSH-Px glutathione peroxidase, an antioxidative enzyme in male acne patients has substantially lower mean activity of erythrocyte GSH-Px than controls.

Inhibition of ROS release has been reported to be of healing value for acne patients.

Miyachi et al. saw that tetracyclines and erythromycin inhibit ROS production of neutrophils and therefore could be efficient in the treatment of acne vulgaris additively by this antioxidant mechanism.  Other researches have shown that subminimal inhibitory concentrations of minocycline and metronidazole, used in the presence of palmitoleic acid, have the antiinflammatory effect of minimizing ROS generated by neutrophils. Akamatsu later reported doxycycline to be the most powerful antioxidant medicine; it minimized ROS in a dosedependent manner. Recently, benzoyl peroxide has been reported to obstruct ROS production of neutrophils. These previous researches support the impact of ROS in the pathogenesis of acne inflammation.

In this research study, reduced activities of Super Oxide Dismutase (SOD) and GSH-Px enzymes in papulopustular acne were found. These enzymes are mostly responsible for antioxidative defense reactions. This finding is consistent with the suspected role of ROS in acne. The increase in ROS due to acne might be responsible for the decrease in SOD and GSH-Px activities.

An inhibitory impact of free radicals on antioxidant enzymes has likewise been reported. Blum et al. revealed that superoxide radicals can prevent the activity of GSH-Px. Singlet oxygen and peroxyl radials prevent the activity of SOD.

We detected reduced GSH-Px activity when catalase (CAT) activities were increasing in the patient group. It has been reported that GSH-Px is more prone to oxyradical inactivation than CAT in moderating the same reaction. It is possible that, as a result of the inhibition of GSH-Px activity caused by acne, H2 O2 will be less quickly oxidised to H2O. Such increased H2O2, the substrate of CAT, and might cause CAT activation. CAT may likewise be enhanced to compensate for the minimized GSH-Px levels.

TBARS, a product of lipid peroxiation, was spotted at insignificantly higher levels in the patient group. It could be that the enzymatic antioxidant system was not completely hindered. Thus, ROS generated by acne swelling might be partly scavenged by the remainder of the antioxidant defense system and might not trigger significantly enhanced lipid peroxidation despite the fact that some antioxidant enzymes were hindered.

The study concludes that the hypothesis of a malfunctioning antioxidant system and hence the therapeutic value of antioxidative compounds in acne is validated. 

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