z-logo
open-access-imgOpen Access
The influence of GSTT/GSTM null genotypes in scarring
Author(s) -
Roxana Flavia Ilieș,
Andreea Cătană,
Radu A. Popp,
Casian Simon Aioanei,
Salomea-Ruth Halmagyi,
I Lukács,
Reka-Eniko Tokes,
Ioana Cristina Rotar,
Ioan Victor Pop
Publication year - 2019
Publication title -
medicine and pharmacy reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.35
H-Index - 16
eISSN - 2668-0572
pISSN - 2602-0807
DOI - 10.15386/mpr-1513
Subject(s) - pathological , scars , medicine , genotyping , genotype , pathology , allele , gastroenterology , physiology , biology , genetics , gene
Background and aims. The process of scarring is a common denominator of interest for the medical field. From general medicine to dentistry, pathological scar tissue represents a challenge in providing optimal care to a patient. The present study aims to investigate whether a systemically reduced antioxidant potential, revealed by null isoforms of glutathione S transferase, affects the process of scarring in a group of female patients. Methods. The study is based on a group of 54 patients with physiological scars after a 6-month observation period, as well as 18 patients with hypertrophic or atrophic scars. Peripheral venous blood was collected, from which DNA was extracted using a commercial kit. Genotyping followed a Multiplex PCR protocol for GSTT1/GSTM1. Results. In a dominant model, the combination of wild type (heterozygous or homozygous) GSTT1 and GSTM1 was negatively associated with pathological scarring, with the wild type (heterozygous or homozygous) GSTM1 genotype being potentially responsible for this effect. Other factors affecting pathological scarring were investigated: family history, phototype, as well as scores on the POSAS and SCAR scales. Conclusions. The presence of GSTT1 and GSTM1 alleles brings forward an increased antioxidant capacity, serving as a protective factor for patients during scar formation.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here