Abstract

Adult growth hormone deficiency (GHD), a condition characterized by increased oxidative stress, is related to augmented cardiovascular, metabolic and oncological risk. A case-control observational study has been performed to evaluate DNA oxidative damage analysing the production of thymidine-glycol in lymphocytes and its correlation with plasma antioxidant levels, evaluated as Total Antioxidant Capacity (TAC). GHD was diagnosed using GHRH 50μg iv+arginine 0,5 g/Kg test, with peak GH response <9 μg/L when BMI was <30 kg/m2 or <4 μg/L when BMI was >30 kg/m2. Three groups were identified: total GHD (n = 16), partial GHD (n = 11), and controls (n = 12). Thymidine-glycol, TAC and IGF-1 have been determined respectively in lymphocytes, plasma and serum samples. When considering thymidine-glycol, we found a significant difference between total vs partial GHD and controls. Unexpectedly thymidine-glycol was lower in total GHD, also accompanied with a significant increase in plasmatic TAC. Our results showed that in adult GHD condition, the production of antioxidant species, in response to increased oxidative stress, could exert a protective effect on thymidine-glycol formation, and consequently on DNA intracellular damages. This pilot study could be inserted in the complex scenario of oxidative damage of GHD, a subtle, yet poorly defined condition, worthy of further insights.

Highlights

  • Adult growth hormone deficiency (GHD) is a clinical syndrome related to low GH secretion by pituitary gland caused by congenital or acquired diseases affecting the hypothalamus-pituitary region [1]

  • The LAG values in total GHD group (t-GHD) significantly differed from partial GHD group (p-GHD) (p = 0.002) and control group (CTRL) (p = 0.0001)

  • When considering ThyG, we found a significant difference between tGHD vs control groups (p = 0.04)

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Summary

Introduction

Adult growth hormone deficiency (GHD) is a clinical syndrome related to low GH secretion by pituitary gland caused by congenital or acquired diseases affecting the hypothalamus-pituitary region [1]. DNA damage and antioxidant response in adult GHD

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