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Summary The acute, sub-acute and chronic toxicity studies on boswellic acids (BAs) were carried out on mice, rats and monkeys. BAs did not cause any mortality in rats and mice when administered orally and intraperitoneally in doses up to 2 g/kg. Daily oral administration of BAs in three doses (low and very high) to rats and monkeys revealed no significant changes in general behaviour, or clinical, haematological, biochemical and pathological data. BAs, therefore, can be regarded as safe for clinical studies.

Attenuation of Benzanthrone Toxicity by Ascorbic Acid in Guinea Pigs. Das, M., Garg, K., Singh, G. B., and Khanna, S. K. (1994). Fundam. Appl. Toxicol. 22, 447-456. Oral administration of benzanthrone (BA) (50 mg/kg body wt/day) to guinea pigs for 30 days resulted in depletion of ascorbic acid (ASA) in the liver, adrenals, and blood serum and in growth retardation (36%) and an increase (18%) in relative liver weight when compared to controls. BA treatment showed a tendency toward normocytic anemia with a decrease in hemoglobin content, reduction in RBC counts, and lowered packed cell volume. Guinea pigs treated with BA showed histopathological changes in liver including fibrosis, bile duct proliferation, and focal necrosis. Testes showed marked damage of seminiferous tubules with vacuolar degeneration and irregular and distorted interstitial spaces. BA showed evidence of patchy glomerular congestion, tubular lesions, and damaged epithelial cells in kidney, while urinary bladders had mild congestion in lamina propia and submucosa. Hepatic GOT, GPT, and LDH were found to be significantly decreased (17.5-33.5%), whereas activities of these enzymes showed a significant elevation in serum of BA-exposed guinea pigs. BA treatment also led to significant decrease of testicular hyaluronidase (29.8%) and LDH (19.8%) and significant depletion of lactic acid content (14.7%). Prior daily oral supplementation with ASA (50 mg/kg body wt) to BA-administered guinea pigs resulted in marked improvement of histopathological and biochemical changes observed in liver, testis, kidney, and urinary bladder of BA-exposed animals. These results suggest that extra supplementation of ASA could attenuate the toxic manifestations of BA.

Modulation of biochemical markers by ascorbic acid was investigated in mice to which benzanthrone (BA) was applied topically (150 nmol/mouse) twice a week for 34 wk. After BA exposure without ascorbic acid, in the skin there were significant decreases in the activities of aryl hydrocarbon hydroxylase (AHH; 38% decrease relative to controls) and ethoxyresorufin-O-deethylase (EROD; 39%), and enhancement of the activities of quinone reductase (41% increase), tyrosinase (82%) and histidine decarboxylase (HDC; 190%). BA exposure also caused significant inhibition of hepatic AHH, EROD and glutathione-S-transferase activities, with concomitant increases in the activities of histidase (52%) and HDC (58%). Ascorbic acid given orally (5 mg/mouse) or topically (1 mg/mouse) twice weekly for 34 wk to BA-treated mice resulted in substantial protection against the effects of BA on these enzyme markers in both the skin and the liver. These results suggest that ascorbic acid could be useful in preventing the biochemical and toxicological manifestations caused by BA in laboratory animals.

Synopsis N-phenyl-p-phenylenediamine (N-PPDA), an industrial intermediate and hair dye ingredient, has been implicated in a variety of toxic symptoms including cutaneous manifestations. However, the role of physiological factors that may determine and modify its absorption and transport within and through the skin is not fully understood. The present study reveals that N-PPDA binds readily to skin showing saturation kinetics with Km and V(max) of 2.54 x 10(-4) M and 4.76 mumol g(-1) skin, respectively. The uptake was dependent upon the area of skin, concentration of the amine, exposure time, temperature and pH of the vehicle. Heat treatment facilitated the binding but temperatures abouv 50 degrees caused significant lowering of the uptake, indicating the possible involvement of collagen matrix. Skin lipids also contributed in the binding of N-PPDA. Bioinhibitors such as KCN, sodium arsenate, NaF, N-ethylmaleimide, cycloheximide, iodoacetic acid and 2,4-dinitrophenol had no effect on the uptake potential, suggesting it to be a non-energy dependent process. Most of the skin-bound N-PPDA was effluxed through serum proteins reaching the target organs via systemic circulation.

The retention and bio-elimination of benzanthrone (BA) in scorbutic and non-scorbutic guinea pigs was investigated to understand the protective role of ascorbic acid. Oral intubation of 14C-BA to scorbutic and non-scorbutic guinea pigs showed a total recovery of around 91% radioactivity through urine, faeces and tissues. Recovery of radiolabelled BA through urine (28%) and faeces (22%) up to 96 hrs averaged 50%, whereas residual radioactivity in liver and testis experienced a recovery of 29% in scorbutic animals. In non-scorbutic animals there was an increased recovery of radioactivity through urine (37%) and faeces (31%) with a decrease in retention (10%) in liver and testis. These results suggest that ascorbic acid facilitates the mobilization and bio-elimination of BA and thereby can decrease the toxicity of the compound.

The design principles that were applied in the design of the integer-RISC machine, are applied to the design of the Reduced Instruction Set Graphics Processor. The processor instruction is defined after critical evaluation of the common graphics operations. Single cycle operations (in a pure RISC style) are performed through instructions for primitive graphics as well as general purpose computations. This processor is envisioned to become the CPU of choice for the ergonomic applications that rely heavily on graphics capabilities for user interface bandwidth improvement. The motivation for integrating graphics with general-purpose computations sterns from the performance enhancement acheived due to increased integration levels, and the program portability offered by a single processor based systems.

The bio-elimination and organ retention of orally administered [ 14 C]benzanthrone, an anthraquinone dye intermediate, were determined in control and ascorbic acid-supplemented guinea pigs. Urinary excretion of benzanthrone in control and ascorbic acid-treated animals during 96 hr was 27.9 and 30.5%, respectively, with peak elimination at 48 hr. Faecal elimination in control and supplemented animals during 96 hr was 24.5 and 38.8%, respectively, with a peak at 48 hr. The organ retention of radiolabelled benzanthrone at the end of 96 hr was of the order of 39% in control animals (gastrointestinal tract 16%; liver 22%; testis 1.2%); ascorbic acid supplementation reduced benzanthrone retention to 19.5% (gastro-intestinal tract 12.7%; liver 6.8%). Overall, pretreatment of guinea pigs with ascorbic acid caused a 32% enhancement in the clearance of radiolabelled benzanthrone through the urine and faeces, while organ retention was reduced by about 50%. A prophylactic dose of ascorbic acid may prevent benzanthrone-induced toxic symptoms in exposed workers.

The bio-elimination and organ retention of [14C]benzanthrone, an anthraquinone dye intermediate, were determined in rats, mice and guinea pigs. Urinary excretion of benzanthrone during 96 hr was higher in guinea pigs (28%) compared with rats and mice (19%). However, faecal elimination during 96 hr was higher in rats (39%) and mice (42%) than in guinea pigs (25%). Urinary elimination of benzanthrone in rats and mice was highest between 12 and 24 hr, while guinea pigs showed a peak value between 24 and 48 hr. The maximum amount of radiolabelled benzanthrone was eliminated through faeces at 24-48 hr in all the three animal species. The retention of [14C]benzanthrone in the liver was comparable in rats (11.2%) and mice (11.9%), while in guinea pigs it was substantially higher (21.9%). The testes of rats and mice were devoid of radioactivity, whereas those of guinea pigs showed a marginal retention (1.25%) of 14C. The present study suggests that guinea pigs are more prone to benzanthrone toxicity than are rats and mice since the bio-elimination of this compound is slower and its organ retention is higher in this species.

Benzanthrone, an anthraquinone dye intermediate, is commonly used for the synthesis of a number of polycyclic vat and disperse dyes. Our prior studies have shown that benzanthrone can be metabolized by rat hepatic microsomal cytochrome P450 (P450) (Biochem. Int., 18, 1989, 1237). In this study, the interaction of benzanthrone with rat hepatic microsomal P-450 and its effect on xenobiotic metabolism have been investigated. Parenteral administration of benzanthrone (40 mg/kg body weight) for 3, 7, or 21 days caused no change in the relative body weight or organ weight of rats. The levels of P450 were found to be reduced (33%-50%) in all the benzanthrone-exposed animals at all the time periods. In vitro addition of benzanthrone caused a spectral change with oxidized P450 and concentration-dependent reduction in the carbon monoxide spectrum of dithionite-reduced P450. The addition of benzanthrone to hepatic microsomes prepared from phenobarbital-treated rats resulted in spectral changes characterized by an absorbance maximum at 397 nm indicative of type I binding. In vitro addition of benzanthrone showed a concentration-dependent inhibition of hepatic aminopyrine N-demethylase (APD) and ethoxyresorufin-O-deethylase (ERD) activities with respective I50 values of 9.5 × 10−4 and 8.0 × 10−5 M. However, the inhibition of aryl hydrocarbon hydroxylase (AHH) even at the highest concentration of benzanthrone (10−2 M), was of the order of only 29%. In vivo administration of benzanthrone also led to the inhibition of APD, AHH, and ERD activities at all treatment times although the magnitude of inhibition was of a lower order. Benzanthrone treatments caused significant depletion of glutathione content with a concomitant enhancement of lipid peroxidation. Also, benzanthrone resulted in a significant inhibition of the cytosolic enzyme, GSH-transferase (23%–34%), although the other enzyme, quinone reductase, which helps in the removal of toxic quinones, was found to be elevated (184%–199%). These results suggest several mechanisms by which benzanthrone may inhibit P450. This impairment of xenobiotic metabolism as well as the enhancement of lipid peroxidation may be relevant to the observed symptoms of benzanthrone-induced hepatotoxicity.

Adult male albino rats were kept on diets containing 0.0, 0.1, 0.5, and 3.0% metanil yellow for 90 days. Various biochemical and histopathological studies were made. Compared to control animals (0.0%), there was no deviation in food intake and growth rate of metanil yellow-fed rats. No pathological change was observed in any of the body organs except the testis. Examination of the testis showed patchy degeneration of seminiferous tubules at a 3.0% dietary level of metanil yellow. Leydig cells showed normal appearance. No change was noted in the cholesterol content of the testis nor in the fructose content of the coagulating glands and dorsal prostate. Acid phosphatase activity in the ventral prostate and alkaline phosphatase in the seminal vesicle remained unaffected. However, decreases in the activities of testicular hyaluronidase, lactic dehydrogenase, and succinic dehydrogenase and in the content of lactic acid were observed.

Studies on the growth of uterine horns and cervix were conducted on 161 prepuberal, puberal and postpuberal (non-gravid) farm-reared buffalo heifers. Age of the buffalo heifers varied between 17 and 37 months, while body weight range was 180–500 kg. The approximate diameters of the mid-cervix and uterine cornua (at the point of pseudobifurcation) were visualized mentally by palpating the organs per rectum with fingers of the left hand while focusing the adjudged diameters between the jaws of a vernier caliper held in the other hand. Both uterus and cervix increased progessively with the advancing age and body weight of heifers, however, the growth of the cervix was more consistent compared to that of the uterus. A marked enlargement in uterine cornua was noted at the time of puberty, however, the rate of cornual growth declined with subsequent estrous cycles.

A total of 24 uterine biopsies were successfully obtained from 40 repeat-breeding buffaloes. The endometrium of 15 buffaloes showed marked neutrophilic infiltration in the epithelium, stroma and uterine glands. In some cases, lymphocyte and plasma cell infiltration, cystic dilatation of the glands and periglandular fibrosis indicated chronicity of the endometritis. Most of the animals (85.0%) had uterine cultures positive for Streptococci, Staphylococci, Gram positive variable cocci, Gram negative bacilli, Anthracoids, and Gram positive bacilli with a predominance of Corynebacteria. With the treatment based on in vitro drug sensitivity tests, 57.1% repeat-breeding buffaloes conceived.

The uptake of benzanthrone by rat skin showed saturation kinetics and was dependent upon the weight of skin and time, temperature and pH of the incubation medium. Heating of segments above 50°C caused significant lowering of the uptake. The uptake was irreversibly inhibited by HgCl2 and not by sodium arsenate, KCN, NaF, p-chloromercuriben zoate, N-ethyl-maleimide, cycloheximide, iodoacetic acid and 2,4-dinitrophenol suggesting that the uptake was not energy-dependent. Lipid micelles of the skin accounted for a part of the binding. Most of the benzanthrone taken up by the skin was effluxed through serum proteins.

Biochemical and histological alterations in lungs, liver, and kidney of albino rats at different time intervals after an intratracheal administration of monazite, the chief source of thorium and some rare earth elements of industrial significance, were investigated. The mild enzymatic and morphological changes observed in the lung suggest an inert behaviour of the monazite dust towards this tissue. However, biochemical alterations in liver and kidney indicate slight dissolution of some constituents of this naturally occurring mineral from the pulmonary tissue to other body organs.

Two experiments, one in the winter (January) and the other in the summer (June), were undertaken to treat anestrous buffaloes at a farm. During experiment I, animals were treated with a progesterone releasing intra-vaginal device (PRID) a , whereas during experiment II, animals were allocated to PRID + GnRH b (125 μg) and GnRH-treated (250 μg). In both the experiments, animals were retained as untreated controls. All the treated animals were clinically examined four days post-treatment and inseminated two or three times at 24-hour intervals. The ovulation and fertility rates of PRID, PRID + GnRH and GnRH-treated animals were 25 and 12 %, 43 and 14 %, and 11 and 0 %, respectively. None of the controls exhibited estrus during the course of the study.

p-Aminodiphenylamine (p-ADPA) has got a binding capacity with tissue proteins. Aspartic and glutamic acids are presumably the responsible units in the protein chain involved in this binding with p-ADPA. p-ADPA is changed into a quinone structure after atmospheric oxidation in Krebs-Ringer-Bicarbonate buffer, pH 7.4 in the presence of trace metal ions. This oxidised form of p-ADPA binds with aspartic acid at pH 7.4 and temperature 40° in 2 hrs. The derivative thus formed absorbs at 450 nm instead of 430 nm.

The effect of benzanthrone on testis and other accessory sex glands in adult male rats was investigated. The weight of the accessory sex glands and testes was unaffected. Acid and alkaline phosphatase activities of seminal vesicles and ventral prostate, fructose content in coagulating gland, and cholesterol in testis remained unchanged. However, testicular hyaluronidase was significantly decreased. Histopathological studies showed patchy degeneration of seminiferous tubules. Leydig cells showed normal appearance. Dorsal and lateral prostates showed typical alveoli with normal secretory activity.

Twenty-one patients with fresh full-thickness burns received a course of two daily applications of sutilains ointment to an area of their burn wound not exceeding 9 per cent of the body surface. Twelve had a mirror-image control burn site of equivalent depth and extent, which was treated identically except sutilains applications were omitted. Good debridement, defined as a wound free of adherent eschar, was observed in 9 patients (43 per cent). The remaining patients' wounds had adherent eschar at the end of the test, or demonstrated equal debridement of both the test and control site. Good debridement was not promoted by increasing the frequency of wet dressings between sutilains applications. Debridement was better in patients receiving more than 8 days of applications. A higher percentage of patients receiving silver sulphadiazine demonstrated good debridement than those receiving gentamicin or no topical antibacterial agent. Burn wound bacterial colonization pattern in sutilainstreated patients did not vary from that observed in those patients receiving only topical antibacterial agents alone. Histological examination revealed that areas with good debridement showed an intense inflammatory cell response and dissolution of the elastic fibres. Control sites and areas with poor debridement showed a lesser inflammatory response and preservation of elastic fibres. No explanation for the variable response to sutilains was apparent histologically. Because of pain associated with application, cost and the unpredictability, sutilains should not be used indiscriminately without monitoring its response carefully and should be used only in conjunction with a topical antibacterial.

Two experiments, one in the villages and one at an organized Government Farm, were undertaken to study the follicular development, ovulation and uterine responses in relation to norgestomet-PMSG treatment (norgestomet ear implant plus 700 IU PMSG at implant removal) in anoestrous buffaloes. The animals were clinically examined 4 days post-treatment. Serum samples for progesterone assay were obtained before the commencement of the treatment and on day 12 after the withdrawal of the treatment. The results demonstrated that treated animals exhibited a good ovarian and uterine response, revealing an overall ovulation rate of 65%; however, the majority of ovulations occurred between 48 and 72 h post-treatment.

Binding affinity of metanil yellow and its breakdown product p‐aminodiphenylamine to serum proteins has been studied employing chromatographic separation on Sephadex G‐200 and by paper and polyacrylamide gel electrophoresis. Metanil yellow has more affinity towards albumin than to globulins. The complexing is presumably through electrostatic forces. p‐Aminodiphenylamine on the other hand, preferably binds to globulin fractions of serum protein. However, a stable binding with BSA alone was also observed. The binding was quite stable and was accompanied by a shift in absorbance from 430 nm to 500 nm. Aspartic acid moiety of protein was found to be one of the units involved in the binding of p‐ADPA to proteins.

Metanil yellow, monoazo C.I. acid yellow 36 (13065), the sodium or calcium salt of m [(p-anilinophenyl)azo]benzenesulfonic acid has been toxicologically classified under category CII by the Joint FAO/WHO Expert Committee on Food Additives. Biotransformation of the dye was studied employing liver slices. When incubated with liver slices under anaerobic conditions, the dye is split at the azo linkage resulting in the formation of metanilic acid and p-aminodiphenylamine.

Metanil yellow, manufactured for textile and other purposes. IS frequently used to colour foodstuffs. A simple and sensitive spectrophotometric method has been developed for the estimation of metanil yellow in foodstuffs and biological tissues. The recovery of metanil yellow is 86.5 % to 96.9 %. Curcumin, bile salts, riboflavin etc. do not interfere. The method is reliable, rapid and the lowest limit of detection is 1 μg. This method can also be applied as a simple colorimetric procedure by reading the colour value in any standard colorimeter using a green filter.

Experimental studies on the effect of poor south Indian diet, alone and in combination with chilli and tamarind, in relation to experimental peptic ulceration have been made over a period of six months. Plasma protein values were not markedly altered in any of the groups at two, four, or six months. Liver protein values were markedly lowered at 4 and 6 months. Ruminai mucosa showed localized proliferation and hyperkeratinization of the stratified squamous epithe in all the groups at four and six months. Ulcerative lesion of grandular mucosa was observed at four and six months in the animals fed on poor south Indian diet in combination with chilli. It has been observed that the damage to the protective mucous barrier is responsible for the production of glandular ulceration.

Dyestuff workers coming in contact with benzanthrone (an intermediate used for the synthesis of a variety of dyes) develop skin lesions, gastritis, liver malfunctions, and sexual disturbances. A highly sensitive fluorometric method to monitor trace quantities of benzanthrone in urine, serum, and biological tissues for experimental studies, has been developed. Coupled with simple extraction and resolution, optimum fluorescence is obtained in an equal mixture of chloroform:methanol, detecting as low as 2 ng benzanthrone. This method is approximately 250 times more sensitive than currently available colorimetric assay.

Intraperitoneally administered benzanthrone (7-H-benz(de)anthracene-7-one) was identified from the urine of experimental rabbits by thin-layer chromatography, and was estimated in urine by the development of a red color at 377 and 335 nm in ether extracts after addition of alcohol and sulfuric acid. All benzanthrone-injected animals had mild vascular congestion in the lamina propria and submucosa of the urinary bladder.

The effect of benzanthrone (an anthraquinone derivative) on blood coagulation in rats has been investigated. Coagulation time, plasma fibrinogen, platelets, pro-thrombin time, bleeding time and serum calcium have been determined in benzan-throne administered animals at 2, 4, 6, 8, 10, 15 and 30 days. Coagulation time was significantly decreased at 2 days of administration and this decrease remained highly significant upto 10 days. The increase in plasma fibrinogen was highly significant from 2 to 6 days. The number of platelets showed an increase at 2 days which be-came highly significant from 4 to 30 days. Bleeding time was significantly reduced at 10 days. Prothrombin time and serum calcium were unaffected.

Benzanthrone, a popular anthraquinone dye-intermediate is known to cause skin and other toxicological manifestations in industrial workers exposed to it. The uptake of benzanthrone through the systemic circulation, in the form of serum protein binding, was characterised by gel filtration and fluorescence quench-ing studies. Fractionation of benzanthrone-protein complex on Sephadex G-200 column revealed that albumin was responsible for the binding with benzanthrone. Addition of benzanthrone quenched the fluorescence intensity of bovine serum al-bumin or human serum albumin with a concomitant enhancement in the fluorescence intensity of benzanthrone. The quenching of albumin fluorescence and the increase in fluorescence of benzanthrone levelled off when the molar ratio of benzanthrone to albumin reached a value of one. This was in accordance with the Scatchard plot analysis. The binding was maximum in the pH range of 7.0-8.0. Stern-Volmer plot showed a linear relationship and downward curving with human serum albumin and bovine serum albumin having an association constant of 6.17 × 105M-1 and 6.54 × 105M-1, respectively. Tryptophan was found to interact with benzanthrone and it also elicited a concentration dependent quenching of its fluorescence with a simultaneous increase in the fluorescence of benzanthrone. The likely involvement in the type II residual tryptophan in the neighbourhood of apolar hydrophobic amino acids of protein chain was anticipated. Binding potential of this dye intermediate with carrier albumin may explain the mode of transport and the ultimate toxicity in the target tissues.

Department of Pharmaceutics, Institute of Technology, Banaras Hindu University,Varanasi-221 005, India. Manuscript received 22 February 1978, revised 4 July 1978, accepted 6 September 1978. A group of Mannich bases of salicylic acid hydrazide have been prepared utilizing different aliphatic, heterocyclic and aromatic amines. These Mannich bases have been tested for antifungal activity against Fusarium oxysporum and Fusarium chlamydosporum. The percentage of colony inhibition are measured, and the results of the tests are tabulated.

A simple, quick and sensitive procedure is described to monitor urinary clearance of aromatic amines in industrial workers. Estimation is based on the measurement of coloured Schiff's bases developed with 4-dimethylaminocinnamaldehyde-organic acid reagent. Extraction of amines in water saturated butanol ensured 89-97% recovery from biological samples with a coefficient of variation of less than 8%. Regression analyses of the absorbance-concentration curves with different aromatic amines showed excellent correlation coefficient and a high molar absorptivity with the lowest detection limits ranging between 0.05-0.12 microgram ml-1. The proposed reagent has additional use as a spray reagent to detect amine spots on chromatograms. Low final acidity ensures estimates of free amines without causing hydrolysis of conjugated amines.

Arsenic, cadmium, chromium, cobalt, copper, lead, manganese, nickel and zinc have been estimated in 18 permitted and 18 non-permitted food colours. Arsenic, chromium, copper and lead were found to be within the maximum allowable international limits in all the permitted colours, but they were in excess in a number of non-permitted colours. There is a case for establishing the maximum allowable concentration (MAC) of cadmium, cobalt, manganese, nickel and zinc in food colours.

1. The effect of clonidine on the direct excitability of hypothalamic, medullary and spinal vasomotor loci has been investigated in cats anaesthetized with chloralose. 2. Clonidine inhibited the excitability of these loci when it was localized to the central sites by intracerebroventricular, intravertebral arterial or intrathecal injection in very low doses (1-2 mug). 3. Topical application of clonidine (0.01 percent and 1.0 percent) to the floor of the fourth ventricle inhibited pressor responses evoked either by stimulation of medullary or hypothalamic vasomotor areas. Inhibition of the pressor responses was accompanied by hypotension and bradycardia in many experiments. 4. It appears that effects of clonidine on the vasomotor loci of the medulla oblongata and the spinal cord contribute to its hypotensive action.

Consumption of edible oils contaminated with Argemone mexicana seed oil is known to cause various clinical manifestations. In the present study, the effect of dietary intake of argemone oil on histopathological changes, haemotological indices and selected marker parameters of toxicity was investigated to observe the exact sites and mode of action of argemone oil in rats. Histopathological changes in the liver showed increased fibrosis, hyperplasia of bile ducts and congestion in a few portal tracts. Lungs of argemone oil-fed animals indicated congestion and thickening of interalveolar septa. Alveolar spaces were disorganised and irregular. Kidneys showed vascular and glomerula congestion and patchy tubular lesions. At 30 days only mild congestion was noted in the myocardium. Cardiac muscle fibres showed degenerative changes at 60 days which were more marked in the auricular wall. Haematological examination showed appearance of anaemia in experimental animals. Hepatic alkaline phosphatase, alanine transaminase and aspartate transaminase activities were inhibited by 30, 29 and 29% after 30 days of argemone intake along with concomitant enhancement in serum by 27, 29 and 66%, respectively. Liver showed decrease in glutathione (32–63%) content along with significant stimulation of lipid peroxidation (49–105%) in argemone-intoxicated animals. These results suggest that liver, lungs, heart and kidneys are the target tissues of argemone oil toxicity and that membrane destruction may be a possible mode of action.

Frequent palpation per rectum was used to delineate patterns of development and atresia of large follicles (> 0.80 cm) on the ovaries of pre-, peri- and postpubertal heifers. The average size of large follicles in prepubertal, peripubertal and postpubertal heifers were 1.25, 1.35 and 1.36 cm, respectively. In 65.39 per cent of the postpubertal heifers, midcycle follicles (> 0.80 cm) could be successfully palpated from day 9 to 13 of the estrous cycle. Moreover, the development and atresia of large follicles in heifers were found to be continuous processes. Follicles were exhibited on the ovaries regularly at intervals of 10–11 days.

The relationships among body weight, height at hook bone, height at pin bone, hip width, rump length, pin width and pelvic area were estimated in puberal (n=50) and two-month pregnant (n=35) Murrah buffalo-heifers. In both types, significant correlations (P angle0.10) existed among all measurements studied. Averages for pelvic area at puberty and two-month pregnancy were 285.05 and 302.00 sq. cm, respectively. At the time of parturition, no buffalo heifer exhibited dystocia due to narrow pelvic opening.

The effect of boswellic acids on bovine serum albumin (BSA)-induced arthritis in rabbits was studied. Oral administration of boswellic acids (25, 50 and 100 mg/kg/day) significantly reduced the population of leucocytes in a BSA-injected knee and changed the electrophoretic pattern of the synovial fluid proteins. The local injection of boswellic acids (5, 10 and 20 mg) into the knee 15 min prior to BSA challenge also significantly reduced the infiltration of leucocytes into the knee joint, reduced the infiltration of leucocytes into the pleural cavity and inhibited the migration of PMN in vitro. The leucocyte-inhibitory activity of boswellic acids was not due to its cytotoxic effect. The boswellic acids did not show any detergent or surfactant properties.

Addition of microgram quantities (5–10 μg per 2 ml) of Mn2+, Fe2+, and Mo2+ increases the intensity of color developed by amino acids two- to three-fold when reacting with ninhydrin. The lowest limit detected by the increased sensitivity of the reaction is 3 nmol of an amino acid. Cd2+, Zn2+, and Al3+ depress the color formation due to reaction between amino acids and ninhydrin. When chromatograms of amino acids are first sprayed with aqueous manganese chloride and later with ninhydrin or with ninhydrin solution containing manganese, not only is the sensitivity increased, but the stained spots retain their color for longer periods.

Workers exposed to dye intermediate, benzanthrone, develop itching, burning sensation, erythema and hyperpigmentation of the skin; which also becomes tender, rough and peals off easily. Earlier experiments have shown that rat skin is capable of picking up benzanthrone. The present study was, therefore, aimed to explore the binding kinetic of skin matrix, of which collagen shares the major proportion. Results revealed that benzanthrone readily binds to reconstituted native collagen fibrils. The uptake is concentration dependent initially and does not in-volve-SH groups. Denaturation (gelatinisation) of collagen by heat or urea treat-ment leads to loss of its binding potential. Serum albumin exhibits a tendency to dissociate benzanthrone prebound to collagen and thus may ultimately assist in efflux of benzanthrone through circulation.