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[Content and dynamics of sulfhydryl compounds in the blood during treatment of diabetes mellitus].

The results of the study of the level of sulfhydryl groups in the whole blood and serum of patients suffering from diabetes mellitus are presented. A total of 170 patients with diabetes mellitus aged from 16 to 70 years were investigated. A severe form of the disease was revealed in 31.2% of the patients, moderately severe in 50.0%, and a mild form--in 18.8%. A significant sulfhydryl groups deficiency (P less than 0.005) was displayed by diabetic patients. The lowest content was found in patients with a severe form of the disease and with ketoacidosis. The existing methods of diabetics treatment failed to completely restore the level of sulfhydril groups. Other additional therapeutic methods are necessary for complete compensation.

Adolescent↗
PubMed1994

Effect of sulfhydryl compounds and glutathione depletion on rat heart myocyte toxicity induced by 4-hydroperoxycyclophosphamide and acrolein in vitro.

Neonatal rat heart myocytes were used to study the acute cardiotoxic effects of cyclophosphamide (CTX) metabolites. The myocytes were equi-sensitive to 4-hydroperoxycyclophosphamide (4HPC) and acrolein in vitro with 50% inhibitory concentrations (IC50) of 123 microM and 152 microM, respectively. The parent compound, CTX, was inactive and the myocytes were much less sensitive to the bis-chloroethylamine alkylator, mechlorethamine (IC50 = 1161 microM). Cellular glutathione (GSH) levels were initially reduced and then transiently elevated following exposure to 4HPC. With acrolein, GSH levels were reduced to unmeasurable levels at all time points. With the addition of 0.5 mM L-buthionine sulfoximine (BSO), myocyte GSH levels were reduced from control values of 120 nmol/mg protein to < 10 nmol/mg protein without causing direct cytotoxicity. However, pretreatment with BSO significantly enhanced the cardiotoxic effects of 4HPC. Finally, two exogenous sulfhydryl-containing compounds were shown to block the myotoxic effects of both 4HPC and acrolein. Mesna and N-acetylcysteine increased at concentrations of 0.01 microgram/ml and 0.1 microgram/ml roughly increased the IC50 of 4HPC by 2-3-fold. These results suggest that acrolein and 4HPC are equipotent cytotoxins and that a transient depletion in GSH accompanies this toxic effect in cardiac myocytes.

Acrolein↗