No abstract

Albino (Sprague-Dawley) and pigmented (Norwegian Brown) male rats were exposed to 2,5-hexanediol (H; 1%) in their drinking water for 5 or 8 weeks, respectively. Half of the rats of each strain were housed in light (average 30 cd/cm2 inside cage, 12 h/day); the other half was kept in constant darkness. Control groups were studied in parallel under identical conditions but without H. Electrophysiological recordings were made 2-5 days and 13 weeks after the end of the exposure to H. Alterations in the visual system, as measured by electroretinography and visual evoked response, were found in groups of albino rats exposed to H and/or light. The pupillary diameter was enlarged in the albino group exposed to both H and light. Among the pigmented rats, alterations were recorded only in the visual evoked response of the H exposed groups. The results demonstrate that simultaneous exposure to H and light can lead to alterations in visual function that are more severe than those induced by each agent alone, and may exceed a simple summation.

Male albino (Sprague Dawley) and pigmented (Norwegian Brown) rats received 1% 2,5-hexanediol (H) in their drinking water for 5 or 8 weeks, respectively. The rats were housed either in 12 h light (average 30 cd/cm2 inside cage) and 12 h darkness (group LH) or in total darkness (group DH). Two control groups (Light only, LC; Darkness only, DC) were studied in parallel under identical conditions. The animals were sacrificed at the end of H exposure or after an ensuing 13-week period without H but under the same lighting conditions. The retinas of albino rats in the LH group showed a reduction (compared to the LC, DH and DC groups) in the number of nuclei per unit area of the outer nuclear layer (ONL; p < 0.05) and degeneration of the outer segment and the inner segment layers (photoreceptor cells). A less pronounced loss of nuclei was seen in the LC group. No decrease in the number of nuclei, or signs of degeneration, were demonstrated in the albino DH or DC groups. Thirteen weeks after exposure to H, the albino LH rats had lost about 50% of the nuclei in the ONL (p < 0.05) and the outer plexiform layer (OPL) had almost disappeared. At the corresponding time, in the pigmented rats the LH and DH groups differed from the LC and DC groups. The degenerative process resulted in no inflammatory changes in the retina. The results imply an interaction exceeding simple summation after exposure to light and H, in destroying photoreceptors and OPL (p < 0.001) in albino rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Exposure to 2,5-hexanedione (2,5-HD), a major n-hexane metabolite, can cause loss of photoreceptor cells, particularly when combined with light energy. The aims of this study were to document the levels of 2,5-HD reached in relation to time in retina, aqueous humor, and serum of the Sprague-Dawley albino rat after: (1) a single oral administration of 2,5-HD (0.04 g/ kg body wt.) by tube feeding; and (2) after subchronic oral administration of 2,5-HD. In addition, morphometric analysis of the retina was carried out to evaluate cell loss at the end of administration and after various periods of recovery. The 2,5-HD concentration in retinal tissue, aqueous humor, and serum reached a peak within 1 h after exposure to a single dose of 2,5-HD. Twenty four hours after the exposure, only a minor amount of 2,5-HD could be detected in the retina and aqueous humor. When 2,5-HD was administered subchronically (0.04 g/kg body wt. per day, for 35 days) no loss of photoreceptor cells was seen immediately after the end of exposure or at the end of a 4-week recovery period. Rats exposed to 0.60 g/kg body wt. per day for 11 days showed no significant loss of photoreceptor cells immediately after the end of exposure but there was a substantial loss of photoreceptor cells after 2 and 4 weeks of recovery. The results demonstrate that 2,5-HD reaches the aqueous humor and retina, and penetrates blood-aqueous humor/retina barriers after oral administration. Moreover, retinal degeneration seen in the animals may be directly caused by 2,5-HD and these changes are dose dependent.

Forty amniotic fluid samples of both sexes were collected in the 16th gestational week and analysed for 17 alpha-hydroxyprogesterone (17-OHP), cortisol, and aldosterone. Hormone concentrations were also analyzed in amniotic fluid of a male fetus postnatally diagnosed as having the salt-losing form of congenital adrenal hyperplasia (CAH). The mother also had CAH of the non-salt-losing type. Hormone concentrations were also determined prenatally in two pregnancies at risk. Amniotic fluid from the pregnancy with the CAH fetus had an approx. six-fold elevated 17 alpha-hydroxyprogester one level, whereas cortisol and aldosterone levels were within the normal range when compared with controls. Hormone concentrations in the two pregnancies at risk were within normal limits and subsequently a healthy boy and a healthy girl were born. Institution of cortisone in the mother during early pregnancy was made in one of the pregnancies. The treatment was withdrawn when normal amniotic hormonal levels were obtained. No sex difference in concentrations of 17-OHP or cortisol was found in the controls, whereas there was a marked sex difference in aldosterone levels (p less than 0.005) with male fetuses having higher concentrations. Diagnosis of CAH in the 16th gestational week can be made by analysing amniotic fluid concentrations of 17 OHP. As cortisol and aldosterone levels were within normal range of the CAH-fetus, they are probably of little use for the prenatal diagnosis of CAH-fetuses/or to differentiate the simple virilizing and the salt-losing forms of CAH. Restriction fragment length polymorphism (RFLP)- analyses of the 21-hydroxylase gene in the fetus gave little further information.