Gonul Vural1, Hesna Bektas1, Sadiye Gumusyayla1, Orhan Deniz1, Murat Alışık2, Ozcan Erel3. 1. a Department of Neurology, School of Medicine , Yildirim Beyazit University , Ankara , Turkey. 2. b Department of Clinical Biochemistry , Atatürk Training and Research Hospital , Ankara , Turkey. 3. c Department of Clinical Biochemistry, School of Medicine , Yildirim Beyazit University , Ankara , Turkey.
Abstract
OBJECTIVE: The objective of this study is to examine thiol-disulphide homeostasis in patients with polyneuropathy dominated by diabetic or non-diabetic axonal degeneration. MATERIALS- METHODS: Fifty-four patients diagnosed with polyneuropathy dominated by axonal damage and 41 healthy subjects were included in the study. The patients were grouped into two groups according to whether or not they had diabetes. The native thiol and total thiol concentrations were measured with the newly developed automated method. RESULTS: While there was no significant difference between the patients with diabetic and non-diabetic polyneuropathy in terms of native thiol and total thiol levels (p > 0.05), the native thiol and total thiol levels of the groups with both diabetic polyneuropathy and non-diabetic polyneuropathy were significantly low compared to the control group (p < 0.01). The level of disulphides in the patients with diabetic polyneuropathy was significantly higher than that of the patients with non-diabetic polyneuropathy and the healthy individuals (p < 0.05). The loss in the sural nerve sensory neural action potential amplitude was positively correlated with the decrease in the levels of both native thiol and total thiol (p < 0.05). DISCUSSION: In our study, we observed that the thiol-disulphide balance was also impaired in patients with non-diabetic polyneuropathy similar to patients with diabetic polyneuropathy, and we therefore considered that impaired the thiol-disulphide homeostasis could be the last common path in patients with polyneuropathy with axonal damage, regardless of the aetiology. Therefore, fortification of thiol deficiency with N-acetyl cysteine or alpha-lipoic acid can fix the thiol-disulphide balance and help decelerate the axonal damage.
OBJECTIVE: The objective of this study is to examine thiol-disulphide homeostasis in patients with polyneuropathy dominated by diabetic or non-diabetic axonal degeneration. MATERIALS- METHODS: Fifty-four patients diagnosed with polyneuropathy dominated by axonal damage and 41 healthy subjects were included in the study. The patients were grouped into two groups according to whether or not they had diabetes. The native thiol and total thiol concentrations were measured with the newly developed automated method. RESULTS: While there was no significant difference between the patients with diabetic and non-diabetic polyneuropathy in terms of native thiol and total thiol levels (p > 0.05), the native thiol and total thiol levels of the groups with both diabetic polyneuropathy and non-diabetic polyneuropathy were significantly low compared to the control group (p < 0.01). The level of disulphides in the patients with diabetic polyneuropathy was significantly higher than that of the patients with non-diabetic polyneuropathy and the healthy individuals (p < 0.05). The loss in the sural nerve sensory neural action potential amplitude was positively correlated with the decrease in the levels of both native thiol and total thiol (p < 0.05). DISCUSSION: In our study, we observed that the thiol-disulphide balance was also impaired in patients with non-diabetic polyneuropathy similar to patients with diabetic polyneuropathy, and we therefore considered that impaired the thiol-disulphide homeostasis could be the last common path in patients with polyneuropathy with axonal damage, regardless of the aetiology. Therefore, fortification of thiol deficiency with N-acetyl cysteine or alpha-lipoic acid can fix the thiol-disulphide balance and help decelerate the axonal damage.