Impact of effluent of Pulp & Paper industry on the flora of river basin at Jaykaypur, Odisha, India and its ecological implications.

The JK Paper industry located at Rayagada discharges biologically untreated effluent more than the permissible limit prescribed by Pollution Control Board, Odisha in to the environment. The industry is seriously polluting the surrounding aquatic and terrestrial environment. No detailed intensive study was carried out by previous workers on this industry earlier. The present study aims at finding out the impact of effluent on the flora at the contaminated site. The chemically treated effluent (TE) contained significant amount of mercury and cadmium. The TE has high BOD, COD, dissolved solids and suspended solids when compared to normal river water at the site of discharge. The TE deteriorated the natural water bodies changing the physico-chemical properties of natural river water. After meeting the river water the TE was diluted after 1 km distance from the meeting point of the river. Crop plants collected from the contaminated site showed higher level of residual Hg and Cd and significant depletion in pigment was observed. Plants collected from both the sides of the treated effluent canal showed significant amount residue mercury and cadmium in the plant leaves. The plants exposed to the TE, showed variation in chlorophyll and Phaeophytin pigment content when compared to their respective control values in all terrestrial plants collected from the contaminated site. In some plant leaves little increment in the pigment level was noted but the values were not significant. The changes observed in the plant pigment might be due to heavy metal accumulation. The presence of residual Hg and Cd in crop plants and plant leaves grazed by grazing animals after absorption, accumulation and enrichment may lead to a possible biological magnification, warrants attention. Proper biological treatment, treatment of effluent by modern methods and removal of heavy metals from the effluent before discharge by the industry is suggested.

Monte Carlo Investigation of Photon Beam Characteristics and its Variation with Incident Electron Beam Parameters for Indigenous Medical Linear Accelerator.

PURPOSE: A Monte Carlo model of a 6 MV medical linear accelerator (linac) unit built indigenously was developed using the BEAMnrc user code of the EGSnrc code system. The model was benchmarked against the measurements. Monte Carlo simulations were carried out for different incident electron beam parameters in the study. MATERIALS AND METHODS: Simulation of indigenously developed linac unit has been carried out using the Monte Carlo based BEAMnrc user-code of the EGSnrc code system. Using the model, percentage depth dose (PDD), and lateral dose profiles were studied using the DOSXYZnrc user code. To identify appropriate electron parameters, three different distributions of electron beam intensity were investigated. For each case, the kinetic energy of the incident electron was varied from 6 to 6.5 MeV (0.1 MeV increment). The calculated dose data were compared against the measurements using the PTW, Germany make RFA dosimetric system (water tank MP3-M and 0.125 cm3 ion chamber). RESULTS: The best fit of incident electron beam parameter was found for the combination of beam energy of 6.2 MeV and circular Gaussian distributed source in X and Y with FWHM of 1.0 mm. PDD and beam profiles (along both X and Y directions) were calculated for the field sizes from 5 cm × 5 cm to 25 cm × 25 cm. The dose difference between the calculated and measured PDD and profile values were under 1%, except for the penumbra region where the maximum deviation was found to be around 2%. CONCLUSIONS: A Monte Carlo model of indigenous linac (6 MV) has been developed and benchmarked against the measured data.

Immunoreactive insulin in rat salivary glands and its dependence on age and serum insulin levels.

The major salivary glands of adult rodents contain immunoreactive insulin (IRI). To determine if the concentration of IRI in salivary glands is modulated by the level of serum insulin, insulin immunoreactivity in the parotid and submandibular glands of male rats at different ages (sucklings, pubescent, mature, and elderly) was assayed and compared with corresponding serum insulin concentrations. Salivary glands from suckling rats contained 94 ng/g (wet weight) insulin, which is 1.6 times higher than the level in pubescent rats, and about 10 times higher than levels in mature and elderly rats. No direct relationship between salivary gland content and serum IRI levels was indicated by the data. In an attempt to increase insulin levels in serum, insulin-secreting pancreatic islet adenomas were induced in young male rats by injecting streptozotocin (an islet tumor-inducing drug) with nicotinamide (which reduces the drug's beta-cell cytotoxicity). The mean insulin content of salivary glands from drug-treated rats that had not yet expressed tumors was no higher than controls. After the development of visible tumors of pancreatic islet tissue, however, salivary gland IRI was markedly elevated, reaching 40 times control levels, whereas serum insulin, and the immunoreactive insulin content of two insulin-sensitive tissues (vis. hepatic, adipose), were elevated only 2-fold. Examination of histologic sections of the parotid and submandibular glands from drug-treated animals revealed no evidence for the formation of salivary tumors. The data indicate that salivary gland insulin content (i) is age-related, being highest in neonates and declining thereafter, (ii) is generally identical in parotid and submandibular glands at a given age, and (iii) is not modulated solely by the animal's serum insulin concentration. These results are discussed in regard to the possible sources of insulin detected in the major salivary glands.

Norms for renal parenchymal volume in Indian children.

Seventy-seven clinically normal children with kidneys of normal size were examined sonographically. Renal parenchymal volumes were calculated and related to age, height, body weight and body surface area; growth charts were constructed. A significant correlation was found between the renal parenchymal volume and the body somatometric parameters. The present report thus provides norms for renal parenchymal volume in Indian children.

Glucose-stimulated hormone release in rats bearing streptozotocin/nicotinamide-induced islet adenomas: evidence for slow and fast responders.

Rats injected with streptozotocin and nicotinamide developed grossly visible islet cell tumors of the pancreas. During i.v. glucose tolerance tests, two populations of tumor-bearing rats were identified: fast responders exhibited significantly lower plasma glucose and markedly elevated plasma immunoreactive insulin (IRI) levels relative to those of the controls. In slow responders, the plasma glucose level was significantly elevated up to 2 h after glucose injection, and the plasma IRI level was lower than that of the controls. During in vitro perfusions with glucose at 300 mg/dl (16.7 mM), tumor-bearing pancreata of fast responders released elevated levels of IRI and immunoreactive somatostatin (IRS); after tumor removal, glucose-stimulated release of these hormones returned to control levels. However, during similar perfusions of pancreata from slow responders, the IRI and IRS release did not decrease after tumor removal, suggesting that the nontumorous pancreatic islets rather than the gross tumors of the slow-responder group were the source of the glucose-stimulated hormone release. These studies demonstrate that gross tumors in the two responder subgroups differ in their glucose-stimulated hormone release.

Glucose modulation of gap junctions in the islets of Langerhans of protein malnourished rats.

It is believed that protein deficiency causes decreased insulin release in response to a glucose stimulus. We have recently shown that in prolonged protein deficiency, decreased insulin response to glucose is directly proportional to a decrease in the islet volume, suggesting no apparent defect in the insulin secretory mechanism in protein deficiency. It is documented that glucose-stimulated insulin release is closely related to an increase in the gap junctions of stimulated islet beta cells. In the present study, we show that the gap junctions of islets obtained from rats fed on a 4% protein diet were increased both in number and size following glucose treatment. This provided further proof that the mechanism to respond to glucose is not compromised in the endocrine tissue of the severely protein malnourished rats.

Impaired macrophage migration in incisors absent (ia) osteopetrotic rats.

Thioglycollate was introduced into the peritoneal cavity of 32-, 50- and 80-day-old normal (ia/+) and incisor absent (ia/ia) osteopetrotic rats, and 3 days later macrophages were harvested. The number of macrophages recovered from 32- and 50-day-old ia rats was significantly less than that elicited from corresponding normal littermates. The macrophages from mutants also showed a significantly impaired ability to migrate in vitro. At 80 days, the number of macrophages obtained from ia rats was not significantly different from those elicited from control rats, and their migratory function was also close to those obtained from controls. The increase in macrophage number and migrating capacity noted in 80-day-old ia rats correlates with increased marrow development at this age as described by Marks (Pathogenesis of osteopetrosis in the ia rat. Reduced bone resorption due to reduced osteoclast function, Am. J Anat 1973;138:165-190.

Toxic effect of lithium in mouse brain.

The effect of lithium ion on glucose oxidation in the cerebrum and cerebellum of mice was measured in vitro by the conversion of isotopic glucose into 14CO2/mg wet weight. Glucose utilization is unaffected by lowest lithium dosage but is inhibited by high lithium concentrations (197-295 mM). Chronic administration of lithium to adult mice decreased the DNA content of the cerebrum and cerebellum at concentrations of 80 and 108 mM. The DNA content of selected postnatal stages of cerebrum and cerebellum was measured starting on Day 1 or 2. This served as another parameter to evaluate glucose oxidation studies at these ages. On the basis of wet weight, both brain parts of neonates of ages 1 and 10 days were approximately one-half that of the adult counterparts. On the basis of DNA content, the cerebrum enhanced its glucose utilization twofold from Day 1 to Day 10 and tripled its utilization from Day 10 to Day 20. The glucose utilization by cerebrum at Day 20 is similar to adult values. In contrast, glucose oxidation in the cerebellum remained relatively constant throughout the postnatal growth. The relative susceptibility of the two brain parts is discussed.

On the origin of induced pancreatic islet tumors: a radioautographic study.

Endocrine tumors of the pancreas are induced in a high percentage of young rats by injections of streptozotocin and nicotinamide (SZ/NA). Benign tumors first appear 20 to 36 weeks after drug injections. To determine the possible site of their origin, the incorporation of [3H]thymidine into islets, ducts, acini, microtumors, and gross tumors was examined by radioautography of histologic sections at 1 to 36 weeks after drug injection. Drug treatment led to early (1- to 6-week) increases in nuclear 3H labeling of exocrine pancreatic structures (ductal and acinar cells), which may involve DNA repair processes. A secondary increase in labeling of duct cells during the period of tumor emergence supports the assumption that SZ/NA-induced tumors are of ductal origin. Microtumors and gross tumors also exhibited markedly elevated rates of [3H]thymidine incorporation compared to control islets. Nontumorous islet tissue, which exhibited a gradual decrease in volume due to B-cell destruction by the drug injection, showed about 10-fold higher 3H labeling than islets of controls at all time points. The results suggest that in addition to ductal precursors, islets that survive SZ/NA-induced injury may also provide sites of focal endocrine cell differentiation to tumor tissue. Once established, both microtumors and gross tumors continue to grow by accelerated cell division.

Morphometric analysis of the endocrine cell composition of rat pancreas following treatment with streptozotocin and nicotinamide.

Using immunohistochemistry and linear scanning, a morphometric analysis was made of the composition of the rat endocrine pancreas at sequential intervals after combined injections of streptozotocin (SZ) and nicotinamide (NA). One week after treatment, the volume of islet tissue was significantly higher than that of the corresponding, saline-injected controls, probably as the result of acute hyperplasia of insulin- and somatostatin-positive cells. However, at all time periods thereafter (6, 20, and 36 weeks), the drug-treated rats showed decreased islet volumes compared to controls. Analysis of aggregate (total) volumes of hormone producing cells at various time periods after drug treatment indicated that decreases in insulin (B-cell) volumes only partially accounted for the observed changes in total islet volume. There were, in addition, early decreases in glucagon (A-cell) and increases in somatostatin (D-cell) volumes. The results suggest that SZ/NA treatment caused limited islet B-cell destruction and transient changes in the proportions of islet A and D cells. Microscopic endocrine tumors were observed at 20 weeks, and both gross and microscopic tumors were observed 36 weeks after SZ/NA treatment. When islet and tumor tissues were included in computation, aggregate volumes of insulin and somatostatin-positive cells were markedly increased, with no significant changes in glucagon-positive cell volumes compared to controls, indicating that the tumors were rich in B and D cells, but poor in A cells. These results are discussed in relation to changes in glucose tolerance and serum insulin levels, and to islet cell volumes following treatment with a diabetogenic dose of streptozotocin alone.

Relation between blood flow and morphology in islet organ of rat pancreas.

By intra-arterial postmortem staining of the pancreas with hematoxylin after the administration of nonradioactive microspheres to anesthetized unfasted rats, the following values (+/-SE) were obtained: mean single islet volume, 1.00 +/- 0.12 nl (median 0.32 +/- 0.04 nl, n = 14); pancreatic intensity of perfusion, 1.18 +/- 0.14 ml X min-1 X g-1 (n = 10); percentage of pancreatic flow to islets, 6 +/- 1% (n = 10); single islet blood flow, 20 +/- 3 ml X min-1 (n = 10); and islet perfusion, 19 +/- 3 ml X min-1 X g-1 (n = 10). Perfusion of islet tissue was calculated to be above average for very small islets and to decrease with increasing islet size to become below average for very large ones. Details of the distribution of the total islet flow to subpopulations of islets grouped according to single islet size are shown pictorially.

Rat pancreatic beta-cells in protein deficiency: a study involving morphometric analysis and alloxan effect.

The possible cause(s) of impaired glucose tolerance in protein-calorie malnutrition was studied. The beta-cell mass was morphometrically determined and the sensitivity to alloxan was characterized in rats fed ad libitum a 4% protein diet, pair-fed or fed ad libitum a 20% protein diet. The percentage of beta-cells in the pancreas was neither affected by protein deficiency nor influenced by caloric intake. However, the diabetogenicity of alloxan was greatly reduced in protein-malnourished rats. This reduction in diabetogenicity by alloxan was partially reversed by feeding animals with sulfhydryl compound. These results suggest that decreased insulin secretion in protein malnutrition is not due to a reduction in beta-cell number.

Uptake and transfer of lithium in pregnancy and lactation in the mouse.

The uptake of lithium in pregnant and lactating mice as well as its transfer to their respective fetuses (18-day postcoitum) and nurslings (11- to 15-day postnatal) were quantified. Lithium carbonate in concentrations of 1 or 2 mg/ml given ad libitum in drinking water produced plasma levels in adults ranging from 0.46 to 1.7 meq/liter. In pregnancy, plasma lithium of the adult was twice that of the fetal plasma. However, there was no statistical difference in brain lithium content between adults and fetuses at the 1- or 2-mg dosage. A significant decrease in bone lithium content was found in fetuses as compared to adults at the 2-mg level. During lactation the plasma lithium of nurslings was one-fourth to one-sixth that of the mothers' plasma. Lithium content in brain and in bone of adults was significantly lower than those of nurslings at both drug concentrations. No apparent effects on adults, fetuses, or nurslings were noted in the short term.

The effect of glucose on insulin and proinsulin synthesis in the streptozotocin-nicotinamide--induced rat islet adenoma.

Studies were conducted to examine the insulin and proinsulin synthetic response to glucose in the streptozotocin-nicotinamide--induced rat islet adenoma. Tumors responded to an increase from 3.8 mmol/L to 16.6 mmol/L glucose by increasing incorporation of [3H]-L-leucine into both proinsulin and insulin. Though this response was statistically significant, the stimulation was less than that noted in rat islets, and the variability of incorporation was greater. In addition, the conversion of proinsulin to insulin was generally slow, again with substantial intertumor variation. The recovery of insulin, as well as proinsulin, was significantly higher at the end of four hours of incubation in tumors incubated in 16.6 mmol/L glucose, implicating an insulin-degradative pathway modulated by glucose. Therefore, while the tumor will not replace conventional sources of tissue for insulin biosynthetic experiments, systems utilizing the tumor can serve as an addition to the methodology for studying previously unrecognized or poorly understood intracellular processes within the beta cell.

The synthesis of insulin and proinsulin in a cell-free system derived from the streptozotocin-nicotinamide--induced rat islet adenoma.

Preliminary studies were conducted to develop a cell-free system for insulin biosynthesis using the streptozotocin-nicotinamide--induced rat islet adenoma. Radiolabeled proteins, migrating on steric exclusion chromatography and SDS-gel electrophoresis in the region of insulin and proinsulin, were synthesized in a system prepared from the tumor 800 X g supernatant fraction, rat liver cytosol, and appropriate energy substrates. The proteins were not synthesized by a rat liver cell-free system, and synthesis could be substantially inhibited by the addition of cycloheximide. In addition, it could be shown that the islet proteins were not the products of residual intact cells within the system, nor were they an artifact due to nonspecific binding of [3H]-L-leucine to pre-existing insulin and proinsulin. The radiolabeled material eluting with insulin on steric exclusion chromatography was identified as [3H]-insulin by immunoaffinity column chromatography.

Teratogenic effects of lithium in mice.

The question of the teratogenicity of lithium carbonate was tested in two inbred strains of mice that are susceptible to teratogens. Strains 129 and A/J mice were treated with varying dosages of lithium carbonate on day 8, 9, or 10, and strain A/J mice were sequentially treated on days 11, 12, and 13 of gestation. Another group of mice of strain 129 were given lithium carbonate in drinking water throughout pregnancy. Levels of lithium were determined in mouse serum (and in brain) of mothers and their offspring with the purpose of comparing equivalent values in mice and in man. A baseline dosage of 0.8 mg of lithium carbonate was chosen, since this dose produced a serum lithium level of 0.8 meq/L, which is comparable to values of patients treated for manic-depressive illness. This baseline dosage or 2 and 4 times this amount did not prove teratogenic in strain 129 mice. However, 5.0 mg (200 mg/kg), which is one-half the LD50 value, caused 41% malformations. The baseline dosage did not cause malformations in strain A/J when given on day 11, 12, or 13 of gestation. Lithium carbonate given in the drinking water to strain 129 mice throughout pregnancy at a concentration that produces serum levels in mice consistent with human values was deleterious. The data suggest that whole or part of total litters were eliminated. The few survivors were apparently normal. Our results suggest that 6 times the therapeutic serum lithium level in humans is teratogenic in mice, as tested by acute experiments. Chronic treatment with a quantity of lithium that produces a serum level equivalent to that of human values is toxic to whole or part of the litters of mice.