Glutathione treatment of dyspermia: effect on the lipoperoxidation process.

We recently introduced reduced glutathione into the therapeutic protocols in some selected cases of dyspermia. This therapy improved semen quality both in a pilot follow-up study and in a double-blind cross-over trial. This improvement was seen in patients with varicocele and germ-free genital tract inflammation, two pathologies in which production of reactive oxygen species or other toxic compounds could have a pathogenic role. Polyunsaturated fatty acids of phospholipids play a major role in membrane constitution and function and are one of the main targets of the lipoperoxidative process. Therefore, to understand the therapeutic action of reduced glutathione, we selected infertile patients and studied the modifications produced by the therapy in seminal parameters, biochemical sperm membrane parameters, and the pattern of fatty acids of phospholipids from blood serum and red blood cell membranes (a model widely accepted as representative of general cell membrane status). The results showed an improvement in both sperm parameters and cell membrane characteristics. This study suggests that biochemical modifications in membrane constitution could explain the seminal results of glutathione therapy. On the other hand, it seems likely that only subjects with systemic membrane disturbances associated with andrological pathologies express this membrane damage in spermatozoa, resulting in dyspermia. This sperm alteration can be partially reversed by glutathione therapy if the structural cell membrane damage is not too severe.

Analysis of polyunsaturated fatty acids in newborn sera: a screening tool for atopic disease?

It has been demonstrated that patients with atopic disease have anomalies of fatty acid composition, as a result of altered metabolism or abnormal incorporation of fatty acids into the tissues. In the present study, in 57 newborns 'at risk' for atopic disease, the polyunsaturated fatty acid (PUFA) levels were found to be lower in cord blood in infants who subsequently developed atopic disease than in non-atopics. In all babies, levels of arachidonic acid and dihomo-gamma-linolenic acid in sera at 1 and 3 months of age were lower than those in cord blood. These changes were more marked in children who subsequently developed atopic disease, and in those who, independently of signs and/or symptoms of atopic disease, were formula-fed. A comparison between IgE and PUFA levels revealed no significant differences at any tested time interval. In conclusion, our data suggest that in children 'at risk' for atopy, PUFA levels may be predictive of atopic disease.

Catecholamines and vitiligo.

The levels of some catecholamine metabolites, namely homovanillic acid (HVA), vanilmandelic acid (VMA), 3-methoxytyramine (MT), normetanephrine (NMN), metanephrine (MN), 3,4-dihydroxy mandelic acid (DOMAC), and 3,4-dihydroxy phenylacetic acid (DOPAC), have been evaluated in the 24 hr urines of 150 patients affected with different types of vitiligo and in 50 healthy age-matched individuals. The patients were divided into three groups according to the different phases of the disease. The first group included subjects affected either with the early active phase or with progressive increase in both number and/or the size of previous lesions. The second group included patients in whom no new lesions had appeared for between 4-8 months. In the third group the white areas had been stable for 1-5 years. The first and second groups showed values of HVA and VMA from 4 to 10 times and from 1/2 to 3 times higher respectively than those of controls, while no significant differences were found between the third group and controls. Our results clearly show that a significant increase of urinary levels of HVA and VMA, deriving respectively from dopamine and from norepinephrine and epinephrine characterizes the onset and the progressive active phases of vitiligo, irrespective of the type of distribution. The increased release of catecholamines from the autonomic nerve endings in the microenvironment of melanocytes in the affected skin areas might be involved in the etiopathogenesis of vitiligo through two main mechanisms: (1) a direct cytotoxic action of catecholamines and/or their o-diphenol catabolites; (2) an indirect action.(ABSTRACT TRUNCATED AT 250 WORDS)