Role of Interleukin-6 and Oxidative Stress in Mentally Retarded patients

Document Type : Original Article

Authors

1 Biochemistry Division, Chemistry Department, Faculty of Science,Mansoura University

2 Genetics Unit, Children Hospital

3 Biochemistry Division, Chemistry Department, Faculty of Science, Mansoura University

4 Micro analytical Unit, Faculty of Science, Mansoura University

Abstract

Abnormalities in thyroid state may result in mental retardation. Oxidative stress and elevated serum inerleukin-6 (IL-6) levels have been identified as an important contributor to neurodegeneration. The aim: This work has been carried out to evaluate the interleukin-6, thyroid hormones as well as some parameters related to oxidative stress in mentally retarded patients with chromosomal abnormalities. Methods: karyotyping for blood, serum thyroid stimulating hormone (TSH), free thyroxin (FT4), superoxide dismutase (SOD), catalase(CAT), malondialdehyde (MDA) and interleukin-6 (IL-6) were measured in 60 mentally retarded patients and 30 healthy volunteers included as control groups. Results: Chromosomal abnormalities were studied in 60 mentally retarded patients, 50 of them were Down's syndromes and the other 10 consisted of (translocations, trisomies, ring chromosome, Edward’s, Patau and Klinefelter syndromes). Thirty three subjects were euthyroid and 27 subjects were hypothyroid. In euthyroid group there was no significant difference in the values of TSH, FT4 and SOD whereas the values of MDA and CAT were significantly higher compared with control. On the other hand, IL-6 levels were highly significantly increased compared with the control group. In hypothyroid group there was a highly significant increase in TSH and IL-6 levels and a highly significant decrease in SOD, CAT, MDA and FT4 levels compared with those of the control group. Conclusion: Increased oxidative stress and IL-6 as well as hypothyroidism are common in mentally retarded individuals with chromosomal abnormalities. These findings are useful in supporting future antioxidant therapies and chemical inhibitors against the function of IL-6 to improve those patients.

Keywords