This study was planned to investigate whether the physiological variations in endogenous gonadal steroid hormones during fertile period to menopause might affect the Arylsulphatase A (ARS-A) activities in leukocytes in healthy women. In premenopausal women, means of the leukocyte ARS-A activity were significantly highest at ovulatory phase, and lowest at early follicular phase. In contrast, the mean leukocyte ARS-A activity in postmenopausal women was approximataely equivalent to the mean leukocyte enzyme in cycling women at early follicular phase in whom the lowest enzymatic activity was observed. The results of our study, therefore, concluded that gonadal steroid released physiologically into the bloodstream might be expected to stimulate the lysosomal system thereby leading to an enhancement in leukocyte ARS-A activity.

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In the present study, the effects of acute ethanol (EtOH) toxicity and of exogenous melatonin (MLT) on this toxicity were examined by measuring membrane-bound ATPases and acetylcholinesterase activities in rat synaptosomal membranes. The concentrations of plasma alpha-tocopherol and adrenal ascorbic acid (AA) were also measured. Synaptosomal Na(+),K(+)-ATPase and Ca(2+)-ATPase activities were significantly depressed in acute EtOH-intoxicated rats compared with controls, while acetylcholinesterase activity remained unaltered. Pretreatment with MLT (10 mg/kg) prior to acute EtOH administration prevented EtOH-induced inhibition of ATPases. Adrenal AA and plasma alpha-tocopherol levels were also depressed regardless of MLT pretreatment. MLT treatment alone affected neither membrane-bound enzyme activities nor tissue and blood levels of vitamins C and E. It is concluded that acute EtOH intoxication disturbs neural transport functions through the membrane-bound ATPase activity depression. Reduced AA and alpha-tocopherol levels may contribute to the neurodegenerative effects of EtOH. However, pretreatment with a high dose of MLT before EtOH administration may be beneficial to prevent EtOH-induced toxicity on ATPase-mediated neural transport functions.

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