Polychlorinated biphenyls affect thyroid function and induce autoimmunity in Sprague-Dawley rats.

Polychlorinated biphenyls (PCBs) have been reported to cause a variety of toxic effects. In order to assess the thyroid function after exposure to PCBs and investigate whether PCBs induce autoimmune process in the thyroid gland, we determined the levels of serum thyroid hormones (FT3, FT4, and T4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) in Sprague-Dawley rats treated with a commercial mixture of PCBs, Aroclor 1,254 (PCBs group), or the antithyroid drug, propylthiouracil (PTU group). The histopathology of the thyroid was also examined. Serum FT3, FT4, and T4 concentrations were significantly reduced, while TSH values were dramatically increased in PCBs group and PTU group compared with control rats (p < 0.05). TPOAb levels were significantly elevated in PCBs-treated rats (p < 0.05) but not in PTU group (p > 0.05). In contrast to the controls, treatment with PCBs lead to distinct histopathological changes in the thyroid gland, such as hyperplasia of the epithelia in follicles, colloid content reduction, vascularization, and lymphocytic infiltration in the perifollicular areas, whereas the major changes in the thyroid in PTU-treated rats were follicles shrinkage or collapse and colloid content reduction compatible with induced hypothyroidism. The results indicate that PCBs affect thyroid function via the induction of autoimmunity, which is a mechanism different from the effect of antithyroid drug on the thyroid gland.

[Studies on the isolation of endogenous sleep factors from Tupaia Belangeri Chinensis (TBC) after sleep deprivation].

The present study was undertaken to explore endogenous sleep factors isolated from 48-72 h sleep deprived (SD) male Tupaia belangeri chinensis (TBC). Only drink ad libitum (10% glucose) was available within 24 h before collection of urine. Controlled "clean" urinary samples were pooled and stored at 20 C. Fraction I-V from the urine were determined after ultrafiltration and Sephadex-G15. Amino-acid analysis of each fraction was automatically done by a 835 Amino-acid Analyzer, respectively. Bioassay was performed in 40 adult rabbits weighing 2.5-3.5 kg of either sex. Experiments were undertaken via the mesodiencephalic intraventricular infusion. Results show that S2C (Fraction-III) (50 micrograms/rabbit, i.c.v.) exhibited significant delta-enhancing effect compared to the controls. Further purification was done with Sephadex G-25 and Sephadex LH-20. The more purified S4B (50 micrograms/rabbit, i.c.v.) also exhibited significant delta-enhancing effect compared to the controls. The amino-acid analysis of Fraction-III revealed that the compositional contents of S2C and S4B are different from what have been known with Factor S, DSIP and SPS.

N-acetyl cysteine enhances the response to interferon-alpha in chronic hepatitis C: a pilot study.

Hepatitis C virus (HCV) is an RNA virus that replicates in both the liver and lymphoid cells. Interferon-alpha (IFN-alpha) is a useful treatment of chronic hepatitis C (CHC) although resistance to this drug occurs frequently. The mechanisms underlying resistance to IFN remain unknown. In this work, we have measured the levels of glutathione in plasma and peripheral lymphoid cells from 15 healthy controls and 24 CHC patients, 10 of whom were without treatment and 14 showed high serum alanine aminotransferase (ALT) values despite therapy with lymphoblastoid IFN for more than 4 months. In all patients, glutathione levels in plasma and in mononuclear cells were depressed in comparison to controls. In IFN-unresponsive patients, the addition of 600 mg tid of oral N-acetyl cysteine (NAC), a glutathione precursor, resulted in a steady decrease of ALT values in all patients, with complete normalization in 41% of cases after 5-6 months of combined therapy. Administration of NAC alone for 1 month was without effect in the 10 patients that were not receiving IFN. Supplementation of IFN with NAC induced a near normalization of intralymphocytic glutathione, but plasma levels were only moderately increased. HCV replication was markedly inhibited in lymphocytes and viremia was cleared in one of the 8 patients tested. In conclusion, NAC enhances the response to IFN in CHC. Controlled studies are needed to ascertain whether antioxidant therapy might act in synergy with IFN in chronic viral hepatitis.