Arylsulphatase A activity and sulphatide concentration in placenta, membranes and cord after delivery

Aim: We evaluated variations in behavior of arylsulphatase A activity (an enzyme that catabolizes sulphatides) and of sulphatide concentration in the placenta, cord and membranes of healthy gravidas at term pregnancy, following spontaneous birth. Methods: We extracted and biochemically determined arylsulphatase A and sulphatide concentration in placenta, cord and membranes (far from and close to internal uterine os) in 14 patients. Results: Activity of arylsulphatase A decreased in the cord, in membranes far from the internal uterine os, in membranes close to the internal uterine os and in the placenta. Sulphatide concentration was minimal in the cord and maximal in placenta, with intermediate values in the membranes. No correlation was found between arylsulphatase A activity and sulphatide concentration, nor among arylsulphatase A activities, nor among sulphatide concentrations among the different tissues. It seems that multiparity may increase and the duration of active labor may decrease arylsulphatase A activity in membranes far from the internal uterine os, while active labor duration does not appear to have any implication on sulphatide concentration in membranes close to the internal uterine os. Conclusions: Arylsulphatase A activities and sulphatide concentrations in fetal adnexa show significant differences.Peer Reviewe

Arylsulphatase A activity and sulphatide concentration in placenta, membranes and cord after delivery

Aim: We evaluated variations in behavior of arylsulphatase A activity (an enzyme that catabolizes sulphatides) and of sulphatide concentration in the placenta, cord and membranes of healthy gravidas at term pregnancy, following spontaneous birth. Methods: We extracted and biochemically determined arylsulphatase A and sulphatide concentration in placenta, cord and membranes (far from and close to internal uterine os) in 14 patients. Results: Activity of arylsulphatase A decreased in the cord, in membranes far from the internal uterine os, in membranes close to the internal uterine os and in the placenta. Sulphatide concentration was minimal in the cord and maximal in placenta, with intermediate values in the membranes. No correlation was found between arylsulphatase A activity and sulphatide concentration, nor among arylsulphatase A activities, nor among sulphatide concentrations among the different tissues. It seems that multiparity may increase and the duration of active labor may decrease arylsulphatase A activity in membranes far from the internal uterine os, while active labor duration does not appear to have any implication on sulphatide concentration in membranes close to the internal uterine os. Conclusions: Arylsulphatase A activities and sulphatide concentrations in fetal adnexa show significant differences.Peer Reviewe

Changes of retinal neurons and glial fibrillary acidic protein immunoreactive astrocytes in spontaneously hypertensive rats

OBJECTIVE: The influence of arterial hypertension on retinal neurons and glial fibrillary acid protein (GFAP) immunoreactive astrocytes was investigated in spontaneously hypertensive rats (SHRs). METHODS: The retinas of 4- and 6-month-old SHRs and age-matched Wistar-Kyoto rats (WKY) were investigated. A group of SHRs, treated from 4 to 6 months with the hypotensive drug hydralazine, was also examined. Microanatomical and immunohistochemical techniques associated with image analysis and the terminal deoxyribonucleotidyl transferase (TdT)-mediated biotin-16-dUTP nick-end labelling (TUNEL) technique for apoptosis or necrosis were used, as well as astrocyte molecular biology (Western blot) techniques. RESULTS: In 4-month-old SHR and WKY rats, retinal morphology and the number of retinal neurons and of GFAP-immunoreactive astrocytes were similar, with the exception of the occurrence of 1% of TUNEL-positive ganglionic neurons in SHRs. In 6-month-old SHRs a decrease of retinal volume and of the number of ganglionic neurons and photoreceptors was observed, compared with age-matched normotensive WKY rats or younger SHR and WKY rats. Two per cent of ganglionic neurons and 5% of photoreceptors were also TUNEL positive. In 6-month-old SHRs, hypertrophic perivascular GFAP-immunoreactive astrocytes were found, whereas their number was unchanged compared to younger cohorts or WKY rats. An increased expression of GFAP was also noticeable in SHRs by Western blot analysis. Hypotensive treatment with hydralazine partly countered retinal changes occurring in SHRs

The hippocampus in spontaneously hypertensive rats: a quantitative microanatomical study

The influence of hypertension on the morphology of hippocampus was assessed in spontaneously hypertensive rats of two, four and six months and in age-matched normotensive Wistar-Kyoto rats. Values of systolic pressure were slightly increased in two-month-old spontaneously hypertensive rats in comparison with age-matched Wistar-Kyoto rats and augmented progressively with age in spontaneously hypertensive rats. No microanatomical changes were observed in the hippocampus of spontaneously hypertensive rats of two months in comparison with age-matched Wistar-Kyoto rats, whereas a decrease of white matter volume was observed in the CA(1) subfield and in the dentate gyrus of four-month-old spontaneously hypertensive rats. In the hippocampus of six-month-old spontaneously hypertensive rats a reduction of grey matter volume both in the CA(1) subfield and in the dentate gyrus, a loss of neurons affecting to a greater extent the CA(1) subfield and an increase of glial fibrillary acid protein-immunoreactive astrocytes was found. The occurrence of apoptosis and/or necrosis identified using the terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick end labelling technique was also observed in the CA(1) subfield and to a lesser extent in the dentate gyrus. The only change noticeable in the CA(3) subfield of six-month-old spontaneously hypertensive rats was a slight increase in the number of glial fibrillary acid protein-immunoreactive astrocytes. These findings indicate the occurrence of neuronal loss and of astrocyte changes in the hippocampus of spontaneously hypertensive rats of six months, being the CA(1) subfield the area most affected. The relevance of these neurodegenerative changes in hypertension and the possible occurrence of apoptosis and/or necrosis as expression of hypertensive brain damage is discussed

Effects of dihydropyridine-type Ca2+ antagonists on the renal arterial tree in spontaneously hypertensive rats

The effects of hypertension and of treatment with dihydropyridine-type Ca2+ antagonists and the vasodilator hydralazine on renal arterial tree were investigated in spontaneously hypertensive rats (SHR) with quantitative microanatomical techniques. Pharmacological treatment decreased to a similar extent systolic blood pressure values in SHR. Increased thickness of the tunica media of intrarenal arteries accompanied and luminal narrowing were observed in control SHR. Lercanidipine, manidipine, and nicardipine significantly countered wall thickening and luminal narrowing. Hydralazine countered luminal narrowing only. Dihydropyridines exerted renal vasocilatory activity primarily on resistance arteries, being lercanidipine the only compound active on small sized arteries

Forebrain white matter in spontaneously hypertensive rats: a quantitative image analysis study.

The volume and the morphology of brain white matter as well as the number and the size of glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes were investigated in 6-month-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto (WKY) rats. The volume of frontal and occipital cortex and of hippocampus was decreased in SHR in comparison with normotensive rats, whereas the volume of neostriatum was unchanged. A remarkable decrease of the volume of internal capsule and striosomes, a moderate reduction of that of corpus callosum and no changes of the volume of external capsule and of white matter of hippocampus were also observed in SHR. In SHR the number of astrocytes was higher in the frontal and occipital cortex and in the white matter of the CA1 and CA3 subfields of the hippocampus, but not in the corpus callosum or in the grey matter of the CA1 and CA3 subfields. Staining for myelin did not reveal alterations in single fibre sheath morphology. These findings indicate the occurrence of changes of forebrain white matter in SHR, consisting in the reduction of it without qualitative modifications of myelinated fibres. The development of gliosis apparently not related with changes of volume of white matter was also found

Sulphatides and arylsulphatase A activity in major salivary glands of hamster (Mesocricetus auratus) after adenocarcinoma induction in oral cavity.

A biochemical study of sulfatides and arylsulfatase A (ASA) was carried out in the submandibular and sublingual glands of the male and female hamster Mesocricetus auratus after experimental induction of oral adenocarcinoma by 7,12-dimethylbenzanthracene (DMBA). Hamster experimental groups included control animals, animals treated with beta-carotene, animals treated with DMBA, and animals treated with DMBA plus beta-carotene. Oral cavity treatment with DMBA induced carcinogenesis in the buccal mucosa, but not in the major salivary glands, where nevertheless, the morphology and expression of both parameters examined changed. In fact, sulfatide concentrations and enzyme activity increased significantly, while in control and beta-carotene-treated hamsters they were similar in both glands and sexes. After administration of DMBA plus beta-carotene, sulfatide concentration decreased, as did ASA activity, slightly in the submandibular gland and remarkably so in the sublingual one of female hamsters. Thin-layer chromatography (TLC) analysis of lipid patterns, after DMBA treatment, revealed considerable differences, not only in sulfatides, but also in other lipid fractions, as well as between the two glands and two sexes. These findings show that oral cavity treatment with DMBA is not able to induce carcinogenesis in the major salivary glands examined; however, it does cause considerable metabolic changes