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Objective To investigate the lung response to traffic-related air pollution by enumerating hemosiderin-laden alveolar macrophages (AM) in sputum. Study design Sputum samples were collected from 103 urban adult males from Calcutta chronically exposed to automobile exhaust. Forty-nine rural individuals served as controls. AM were identified by nonspecific esterase staining. Perl's Prussian blue technique was employed for the detection of hemosiderin-laden AM (siderophages). Results The urban group, consisting of 31 traffic officers, 25 automobile service station workers and 47 street hawkers, had seven times more AM in their sputum than did the matched controls. Besides, a remarkable rise (27-fold) in the number of siderophages in sputum was observed in urban individuals. Smoking further elevated the AM count and number of siderophages. Conclusion Abundant siderophages in the urban group may indicate the toxic effect of airborne pollutants on the lung, leading to phagocytosis of destroyed cells, including erythrocytes, and accumulation of iron in AM. Enumeration of siderophages in sputum appears to be a simple, noninvasive, inexpensive cytochemical technique well suited to preliminary assessment of the adverse effects of air pollution on the lungs in large, population-based studies, especially in developing countries.

1. No difference was observed in thein vitro growing ability of granule cells isolated from hypothyroid or normal rat brain. When granule cells were taken from hypothyroid rat brain and grown in normal culture medium containing 10% fetal calf serum, they behaved similarly to the granule cells obtained from normal rat brain. 2. In both cases there were progressive losses ofin vitro growing ability of the granule cells with the age of the animal and it became impossible to grow them when derived from 21 days or older animals. 3. A marked decrease in cell surface GM1 was observed when the cells were maintained under thyroid hormone-deficient conditions in culture. 4. Anti-GM1 antibody was found to inhibit significantly the migration of granule cells along the astrocyte fibers. 5. These results indicate that GM1 has an important role in thyroid hormone-dependent postnatal brain maturation in rat.

Lindane (γ-HCH) given to adult female mice orally at various doses and over varying periods adversely affected adrenocortical function. Adrenal weights decreased and both fasciculata and reticularis zones markedly regressed. Histopathological lesions were also noted and plasma and glandular glucocorticoid contents were significantly reduced. Simultaneously an increase in cholesterol and a decrease in ascorbic acid content of the adrenal glands were noticed. The adrenotoxic effect of this chlorinated insecticide possibly results from depressed corticoid production in situ and /or suppressed activity of enzyme(s) that catalyze the peripheral transformation of steroids.

The expression of specific UDP-glucuronosyltransferase isoforms in 2-acetylaminofluorane—induced rat liver preneoplastic nodules was studied; livers from pair-fed littermates were used as controls. For comparison, liver and kidney from 3-methylcholanthrene—treated or untreated (control) rats were used. Steadystate UDP-glucuronosyltransferase mRNA levels were determined by Northern blot analysis or in situ hybridization of tissue sections using a 30-mer oligonucleotide specific for the 3-methylcholanthrene—inducible UDP-glucuronosyltransferase (which is active toward 4-nitrophenol) or a double-stranded cDNA probe specific for androsterone—UDP-glucuronosyltransferase. For 3-methylcholanthrene—inducible UDP-glucurono-syltransferase, the mRNA level was very low in control liver; there was a 15-fold increase after 3-methylcholanthrene treatment. This mRNA was present at relatively high concentration in the kidney and there was a threefold increase after 3-methylcholanthrene administration. In livers with preneoplastic nodules 1 mo after cessation of carcinogen administration, this mRNA concentration was approximately 15 times greater than in control liver. Similar changes in the level of the 3-methylcholanthrene—inducible UDP-glucuronosyltransferase were also observed by in situ hybridization of tissue sections. Immunocytochemical studies using an antiserum that recognizes the 3-methylcholanthrene–inducible UDP-glucuronosyltransferase showed a marked increase in the concentration of this isoform in preneoplastic nodules compared with the adjacent nonnodular liver. Consistent with the changes in mRNA levels, there was a threefold increase in 4-nitrophenol–UDP-glucuronosyltransferase activity in 3-methylcholanthrene–treated rat livers and in livers with preneoplastic nodules. In contrast to the 3-methyl-cholanthrene–inducible UDP-glucuronosyltransferase mRNA, the androsterone–UDP-glucuronosyltransferase mRNA was abundant in the liver and nearly absent in the kidney; its concentration was not increased after 3-methylcholanthrene administration or in preneoplastic nodules. Immunocytochemical studies using an antiserum that recognizes androsterone- testosterone– and bilirubin–UDP-glucuronosyltransferase isoforms did not show any increase of the concentration of these antigens in preneoplastic nodules. Similarly, activities for androsterone, testosterone and bilirubin also did not increase after 3-methylcholanthrene administration or in livers bearing the preneoplastic nodules. (HEPATOLOGY 1991;13:38—46).

Isolated cryopreserved human liver cells, attached to collagen-coated microcarriers, were injected intraperitoneally into mutant rat recipients genetically deficient in either bilirubin uridine diphosphoglucuronosyltransferase activity (Gunn rats) or albumin synthesis (Nagase analbuminemic rats). One group of the recipient Gunn and analbuminemic rats were made genetically immunodeficient by interbreeding with athymic rats with inherited T-cell deficiency. Injected microcarriers and cells formed aggregates on the surface of the pancreas. There was no morphologic evidence of rejection in athymic recipients, whereas immunocompetent recipients demonstrated rejection within 5 days of transplantation. Athymic-Gunn rat recipients demonstrated excretion of bilirubin glucuronides in bile for 30 days and reduction in their serum bilirubin levels. In recipient athymic-analbuminemic rats, plasma albumin levels increased from pretransplantation levels of 0.025–0.05 mg/ml to 3.9–4.8 mg/ml 8 days posttransplantation and remained nearly at that level throughout the 30 days of the study. A method of harvesting, attaching to microcarriers, cryopreserving, and in vivo testing of human hepatocytes with prolonged survival and function in athymic-Gunn and athymic-analbuminemic hybrid rats is reported. These rats are excellent animal models for testing xenograft function.

Partial purification of the dihydropyridine receptor from rat skeletal muscle demonstrated mainly a 60 kDa band in SDS-polyacrylamide gel. An antibody raised against that protein behaved as a calcium channel agonist viz. Bay K8644. The affinity purified antibody, when added to cultured heart cells, increased the beat rate 40–80% depending on the titer of the antiserum. The antibody also woke up the beats of the cells previously blocked with the channel antagonist, nifedipine. Immunoblot analysis indicated that the receptor of this antibody in heart cell membrane is also a 60 kDa protein.

Lindane (gamma-hexachlorocyclohexane) was administered to laying ducks (Anas platyrhynchos domesticus) in 3 doses viz. (1) 20 mg/kg body weight daily, (2) 20 mg/kg body weight thrice weekly and (3) 20 mg/kg body weight twice weekly for 8 weeks. Egg laying was immediately stopped for 3 weeks in the first 2 groups and when resumed it became highly irregular with clutch size drastically reduced (1 against 7 of control ducks). The initial delay was absent in the 3rd group and reduction in clutch size was also marginal (5 against 7). Laying frequencies were 8.3%, 11.7% and 40% in Groups 1, 2 and 3 birds respectively against 50% frequency of the normal ducks. Hepatic, plasma and ovarian vitellogenin levels were substantially reduced in the first 2 groups. At the same time liver RNA level was markedly reduced. Ovary of such birds lack mature vitellogenic follicles and the thecal layer of moderately differentiated oocytes became highly atrophic. Stilbestrol (50 mg/kg body wt--single injection) administration to lindane fed pauci-layer ducks restored egg laying within 24 h, with return of a normal level of plasma vitellogenin and hepatic RNA. The results suggest that lindane induced estradiol insufficiency causes inhibition of hepatic RNA and yolk protein synthesis, thereby preventing transformation of moderately differentiated oocytes to mature vitellogenic follicles, delaying ovulation and thus drastically reducing clutch size.