bluuebunny/crossref_metadata_2025_split huggingface dataset:
Triorganotin inhibition of rat cardiac adenosine triphosphatases and catecholamine binding
Authors: Cameron Joseph A. , Kodavanti Prasada Rao S. , Pentyala Srinivas N. , Desaiah Durisala 
Published: October 2006

AbstractTriorganotins have been reported to affect heme metabolism as well as the cardiovascular system. Our recent studies indicated that these organotins inhibit cardiac sarcoplasmic reticulum Ca2+‐transport and cAMP‐stimulated phosphorylation of specific proteins involved in Ca2+ transport, suggesting their interference with cardiac adrenergic function. The present study determines the effect of three organotins–tributyltin bromide (TBT), triethyltin bromide (TET) and trimethyltin chloride (TMT)–on rat cardiac ATPases and catecholamine binding, since these phenomena are involved in cardiac function. Cardiac membrane fraction was prepared from heart ventricles of male Sprague‐Dawley rats. All three organotins inhibited cardiac Na+,K+‐ATPase, [3H]ouabain binding, K+‐activated p‐nitrophenyl phosphatase (K+‐PNPPase) and oligomycin‐sensitive (OS) and oligomycin‐insensitive (OI) Mg2+‐ATPase in a concentration‐dependent manner. K+‐PNPPase was less sensitive to these triorganotins when compared to Na+K+‐ATPase, suggesting that triorganotins affect the Na+‐pump activity by acting on the Na+‐dependent phosphorylation process. OS Mg2+‐ATPase was more sensitive to these organotins when compared to OI Mg2+‐ATPase, confirming their potent effect on the enzymes of oxidative phosphorylation. The order of potency is TBT > TET > TMT. TET and TMT, but not TBT, inhibited [3H]norepinephrine and [3H]dopamine binding to cardiac membranes in a concentration‐dependent manner, the effect being more with TET. These results suggest that triorganotins inhibit sodium pump activity as well as ATP synthesis. Since Na+,K+‐ATPase is involved in the active transport of catecholamines, triorganotins not only inhibited the catecholamine transport but also to some extent affected catecholamine binding, thus interfering with cardiac function.
Effects of some organophosphorus compounds on the binding of a radioligand (8‐cyclopentyl 1, 3‐[3H]dipropylxanthine) to adenosine receptors in ovine cardiac membranes
Authors: Lau Wai‐Man , Szilagyi Maria , Freeman Shirley E. 
Published: October 2006

Abstract8‐Cyclopentyl‐1,3‐[3H] dipropylxanthine ([3H]CPX) is a potent radioligand that specifically binds to the A1 adenosine receptors. Its high specificity makes it a suitable ligand for the characterization of A1 adenosine receptors in tissues with low receptor densities. We have demonstrated that the organophosphorus compounds soman, tabun and sarin, at relatively high concentrations, all bind to the A1 adenosine receptors in ovine cardiac membranes with Ki values of 36.7, 328 and 175 μM, respectively. The binding of soman to the receptor site was found to be totally reversible. We suggested that these organophosphorus compounds affect the mechanical responses of the heart through interaction with a potassium channel that does not seem to be closely linked to the A1 adenosine receptors.
Validation of a non‐invasive technique to assess immediate or delayed onset of airway hypersensitivity in guinea‐pigs
Authors: Pauluhn J. , Eben A. 
Published: October 2006

AbstractConscious Hartley guinea‐pigs were sensitized with trimellitic anhydride (TMA) or trimeric hexamethylene diisocyanate biuret (Des‐N) by repeated intradermal injections or by inhalation exposure. Immediate‐ and delayed‐onset pulmonary reactions were recorded during/after challenges with the hapten or protein conjugate of the hapten, respectively. The positive control was sensitized and challenged with ovalbumin (OA) by inhalation. Homocytotropic antibodies of the IgGI type were determined to correlate antibody titres and pulmonary responses. Immediate‐onset pulmonary reactions were apparent in guinea‐pigs sensitized by inhalation of TMA and OA. Animals sensitized intradermally with TMA demonstrated more vigorous immediate‐onset reactions than animals sensitized by inhalation. The measurement of breathing parameters demonstrated that the ability to detect immediate‐onset airway hyperreactivity was best when the breathing rate and tidal and minute volumes were measured. None of the measurements for delayed‐onset reactions presented conclusive results, since sensitized as well as naive guinea‐pigs demonstrated a delayed increase of breathing frequency. Antigen‐specific IgG1 antibodies were several orders of magnitude higher in intradermally sensitized animals compared with animals sensitized by inhalation. Although Des‐N‐sensitized guinea‐pigs experienced high IgG1‐antibody titres, no response of pulmonary hypersensitivity could be elicited after hapten or conjugate challenge. In summary, it would appear that pulmonary hypersensitivity depends on factors other than IgGl antibody titres. For the screening of chemicals, the dermal induction and inhalation challenge protocol was revealed to be more sensitive than the inhalation induction and inhalation challenge protocol.
Depression of iron uptake into erythrocytes in mice by treatment with the combined benzene metabolites p‐benzoquinone, muconaldehyde and hydroquinone
Authors: Guy Robert L. , Hu Peidi , Witz Gisela , Goldstein Bernard D. , Snydert Robert 
Published: October 2006

AbstractUsing radio‐iron uptake into erythrocytes as a measure of hematopoiesis, it was demonstrated that p‐benzoquinone (BQ) and muconaldehyde (MUC) are potent inhibitors of bone marrow function in female mice. These two benzene metabolites reduced iron uptake at dosages of <5–6 mg kg−1. The combination of MUC and hydroquinone (HQ) (100 mg kg−1) was additive, reducing iron incorporation to an extent that was the sum of the effect of each chemical given alone. The combined effect of MUC and BQ was significantly less than additive, demonstrating antagonism in the response. Multiple regression was used to study the contributions of the components of binary mixtures of the benzene metabolites (METAB). Data obtained from standard curves of METAB and their mixtures are separable in regression analysis. Thus, for zero interaction of METAB, the responses would be simply additive, while positive and negative interaction would indicate synergy and antagonism, respectively. T‐testing of the data resulted in non‐significant values for the mixture MUC+HQ, indicating zero interaction and an additive response. The negative t‐values obtained for the mixture MUC + BQ, however, indicate negative interaction or an antagonistic response. Since mutually exclusive agents share the same binding sites and occupation of a site by one agent excludes its occupation by another, they cannot interact in producing the effect; combinations of these agents show zero interaction and are simply additive. This suggests that HQ and MUC are mutually exclusive and share the same binding site. Conversely, MUC and BQ are mutually non‐exclusive and this requires the presence of at least two binding sites. These results support the hypothesis that the toxic effects of benzene are produced by several metabolites acting interactively.
Comparative studies of in vitro renal cephaloridine toxicity between normoglycemic and diabetic rats
Authors: Valentovic Monica A. , Jeffrey William , Ball John G. , Bailly Dianne , Morenas Mario , Kinder Jack 
Published: October 2006

AbstractThis study investigated if the attenuation in cephaloridine toxicity associated with streptozotocin (STZ)‐induced diabetes can be attributed to a direct cellular effect. Comparative studies examined the direct toxicity of cephaloridine 14 days after (35 mg kg−1, i.p.) STZ or vehicle injection of male Fischer 344 (F344) rats. In vitro cephaloridine toxicity was assessed by measuring lipid peroxidation, renal gluconeogenesis and organic ion accumulation in renal cortical slices. The in vitro toxicity of cephaloridine was reduced in the diabetic group since lipid peroxidation was not increased following a 120‐min exposure to cephaloridine. This was in contrast to a concentration‐ and time‐dependent increase in lipid peroxidation in renal tissue derived from normoglycemic animals pre‐incubated with 0–5 mM cephaloridine. Renal gluconeogenesis was inhibited in a concentration‐dependent manner in the normoglycemic group following a 15–90‐min exposure to 0–5 mM cephaloridine. Pyruvate‐stimulated gluconeogenesis was diminished in the diabetic group only after a 90‐min preincubation. Renal cortical slice accumulation of p‐aminohippurate (PAH) and tetraethylammonium (TEA) was decreased in the normoglycemic group. Accumulation of TEA, but not PAH, was decreased (P < 0.05) in the diabetic group. These results indicate that in vitro cephaloridine toxicity was attenuated by STZ‐induced diabetes.
Effects of subacute pyridostigmine administration on mammalian skeletal muscle function
Authors: Adler Michael , Deshpande Sharad S. , Foster Robert E. , Maxwell Donald M. , Albuquerque Edson X. 
Published: October 2006

AbstractThe subacute effects of pyridostigmine bromide were investigated on the contractile properties of rat extensor digitorum longus (EDL) and diaphragm muscles. The cholinesterase inhibitor was delivered via subcutaneously implanted osmotic minipumps (Alzet®) at 9 μg h−1 (low dose) or 60 μg h−1 (high dose). Animals receiving high‐dose pyridostigmine pumps exhibited marked alterations in muscle properties within the first day of exposure that persisted for the remaining 13 days. With 0.1 Hz stimulation, EDL twitch tensions of treated animals were elevated relative to control. Repetitive stimulation at frequencies >1 Hz led a use‐dependent depression in the amplitude of successive twitches during the train. Recovery from pyridostigmine was essentially complete by 1 day of withdrawal. Rats implanted with low‐dose pyridostigmine pumps showed little or no alteration of in vivo twitch tensions during the entire 14 days of treatment.Diaphragm and EDL muscles excised from pyridostigmine‐treated rats and tested in vitro showed no significant alterations in twitch and tetanic tensions and displayed the same sensitivity as muscles of control animals to subsequent pyridostigmine exposures. In the presence of atropine, subacutely administered pyridostigmine protected rats from two LD50 doses of the irreversible cholinesterase inhibitor, soman. In the absence of atropine, the LD50 of soman was not altered by subacute pyridostigmine treatment.
Acute toxicity of 2‐butyne‐1,4‐diol in laboratory animals
Authors: Jedrychowski Ryszard A. , Czajkowska Teresa , Stetkiewicz Jan , Stetkiewicz Irena 
Published: October 2006

AbstractAcute toxicity of 2‐butyne‐1, 4‐diol (BYD) was evaluated in laboratory animals. The evaluation involved acute oral and dermal toxicity in rats, dermal and ocular irritation in rabbits and skin sensitization in guinea pigs. The oral LD50 values for BYD were 132 mg kg−1 in male rats and 176 mg kg−1 in female rats. Post‐mortem histology showed severe damage in lungs, liver and kidneys. In surviving rats, moderate to severe degenerative changes were observed in the liver but only mild lesions in the kidneys. In acute dermal toxicity studies the test chemical was applied either as a solid substance or as 40% aqueous solution at a dose of 5 g kg−1 for 24 h. Within 48 h of application of the diluted test material, half of the rats died. Liver and kidneys were the primary targets and different stages of degeneration, including necrosis, were observed. No deaths occurred after application of the solid substance. In rabbits, BYD was slightly irritant to skin and eyes. No allergic contact dermatitis was observed in guinea pigs.
Flow cytometry, morphometry and histopathology as biomarkers of benzo[a]pyrene exposure in brown bullheads (ameiurus nebulosus)
Authors: Grady Andrew W. , McLaughlin Ronald M. , Caldwell Charles W. , Schmitt Christopher J. , Stalling David L. 
Published: October 2006

AbstractBrown bullheads were given a single intraperitoneal dose of 0, 5, 25 or 125 mg kg−1 benzo[a]pyrene (BaP), a carcinogenic polycyclic aromatic hydrocarbon, and evaluated over 18 months. Flow cytometric analyses of hepatocyte DNA content indicated an increase in DNA synthesis in BaP‐exposed fish prior to day 14 post‐exposure. Thereafter, all flow cytometric variables returned to initial levels. Histopathological evaluation of livers from fish sampled at 18 months revealed significant differences among treatments in the amount of hepatic macrophage ceroid pigmentation and basophilic staining intensity. No neoplasms or changes in blood cell DNA content were detected. Significant morphometric variations existed among fish, but differences between sexes overshadowed differences attributable to dose. Flow cytometry yielded no evidence of long‐term DNA alterations from a single exposure to BaP; however, the differences detected by DNA analysis shortly after the toxic event suggest that flow cytometric cell cycle analysis may be useful for documenting continuing exposures.
Tannin content of tea and coffee
Authors: Savolainen H. 
Published: October 2006

AbstractThe tannin content of over‐the‐counter Indian tea, of green coffee beans and of the roasted coffee beans prepared from the same green beans was determined with a radial diffusion ‐ protein precipitation technique and with a spectrophotometric method. The green beans contained 6.6 ± 0.6 mg g−1 weight tannic acid equivalents as found by protein precipitation (n = 5, ± SD) or 6.8 ± 2.3 mg g−1 by spectrophotometry. The same figures for roasted beans were 18 ± 1.7 and 17 ± 2.7 mg g−1, respectively. Tea contained 37 ± 2.6 mg g−1 weight tannic acid equivalents as analysed by spectrophotometry and 24 ± 2.8 mg g−1 by the protein precipitation technique. The latter finding may show that the biological reactivity of tannins is variable, although no major changes in the tannin‐precipitated albumin occurred as shown by electrophoretic analysis. Both methods provide an easy analysis of the reportedly carcinogenic plant tannins.
Comparative lethality of methanol, ethanol and mixtures in female rats
Authors: Youssef Ashraf , Madkour Kadri , Cox Chris , Weiss Bernard 
Published: October 2006

AbstractThe lethalities of pure methanol and pure ethanol were compared to two mixtures of ethanol/methanol with the following percentages (95/5% and 65/35% v/v). This study was conducted to simulate situations of human exposure to denaturated alcohol (by 5% methanol) or adulterated alcohol (by 35% methanol). Four groups of female adult virgin albino rats were treated with the four mixtures. A fifth group was used as a vehicle control. Graded oral doses were given to eight animals per dose. Lethality over 24 h was used as an endpoint. The LD50 was calculated for each of the four treatments on a molar basis. A dose‐response function for each mixture was plotted of percentage lethality vs. mmol kg−1 equivalent to the given ml kg−1 dose. Results showed a significantly different LD50 estimates (P < 0.03) for the four mixtures. The order of lethal toxicity was as follows: 95/5% methanol/ethanol, pure methanol, pure ethanol then 65/35% methanol/ethanol. Slope comparisons indicated two pairs: 65/35% ethanol/methanol and pure ethanol yielding a steep slope, and 95/5% ethanol/methanol and pure methanol yielding a shallow slope. These data indicated that the acute lethality of ethanol/methanol mixtures is a complex unpredictable function. This toxicity presumably depends in a complicated way on the differences in the effective molecular weights of the two alcohols in each of the mixtures.
The effects of cyanide on brain mitochondrial cytochrome oxidase and respiratory activities
Authors: Pettersen John C. , Cohen Steven D. 
Published: October 2006

AbstractBrain mitochondrial cytochrome oxidase and respiratory activities were compared after in vivo and in vitro exposure to cyanide. For the in vivo studies, mice were exposed to a non‐lethal (4 mg kg−1) or lethal (20 mg kg−1) dose of KCN. From these mice, purified brain mitochondria were prepared and cytochrome oxidase and respiratory activities measured. Results of these experiments revealed greater inhibition of cytochrome oxidase activity following a lethal (20 mg kg−1) than a non‐lethal (4 mg kg−1) KCN dose (57 and 45% inhibition, respectively). Respiration states 3 and 4 of brain mitochondria prepared from mice that received 4 mg kg−1 KCN were inhibted by 15 and 20%, respectively. In mice that received a lethal 20 mg kg−1 KCN dose, respiration states 3 and 4 were each inhibited by ca. 30% (P<0.05). In vitro, mitochondrial cytochrome oxidase activity was inhibited in a concentration‐dependent fashion at cyanide concentrations of 10−6–10−2 M. A biphasic inhibition of ADP‐stimulated (state 3) respiration was observed. Cyanide concentrations of 10−6–10−4 M produced only a 25% inhibition of respiration state 3, whereas 10−3 M produced 80% inhibition. Because this dramatic inhibition only occurred at cyanide concentrations that caused >50% inhibition of mitochondrial cytochrome oxidase activity, these findings suggest that a large proportion of cytochrome oxidase activity may be functional reserve and that cyanide poisoning likely involves other mechanisms in addition to inhibition of cytochrome oxidase.
Comparative study on the effects of five benzoylphenylurea insecticides on haematological parameters in rats
Authors: Tasheva Maria , Hristeva Vessela 
Published: October 2006

AbstractFive benzoylphenylurea insecticides were administered to male Wistar rats for 28 days at oral doses of 100 mg kg−1 each. Elevation of methaemoglobin was found only in the diflubenzuron‐ and triflumuron treated groups. The number of reticulocytes was increased in all of the treated groups.
Possible Examples of Chemical Hormesis in a Previously Published Study
Authors: Calabrese Edward J. , Baldwin Linda A. 
Published: October 2006

AbstractA re‐examination of data presented by Daston et al. provided an opportunity to assess the occurrence of chemical hormesis due to the wide dosage range tested and to the large number of treatments within the dosage range. The data revealed numerous examples of possible chemical hormesis for a variety of end‐points measured.
Texicological evaluation of mixtures of ten widely used pesticides
Authors: Chaturved Arvind K. 
Published: October 2006

AbstractToxicities of pesticidal mixtures in biological systems have not been explored adequately. Therefore, mixtures of ten widely used pesticides were evaluated for their toxicity in ICR male mice (21–24 g). Mice were given four mixtures of alachlor, aldrin, atrazine, 2,4‐dichlorophenoxyacetic acid, DDT, dieldrin, endosulfan, lindane, parathion and toxaphene, at 0.01, 0.1, 1.0 and 10 ppm of each of these pesticides, in drinking water for 90 days ad libitum. Also, two mixtures at 2.5 and 5 mg kg−1 of each pesticide in 7.5% Tween‐80 in water were administered to additional groups of mice by oral intubation daily for up to 14 days. In relation to the control, the 90‐day exposure caused a dose‐dependent increase in the liver/body weight ratio (3–44%), a decrease in the pentobarbital (60 mg kg−1, i.p.)‐induced sleep time (11–79%) and an increase in the metabolism of aniline (233–399%), amidopyrine (79–231%), phenacetin (127–318%) and benzo[aIpyrene (286–1633%)] in the 9000 g hepatic supernatants from the mixture‐treated mice. Proliferation, dilatation and fragmentation of the endoplasmic reticulum and scattering of ribosomes were noticed with mixture livers. In the 5 mg kg−1 group, 90% of the animals died by Day 8; incidence of death was considerably less in the 2.5 mg kg−1 group. The serum cholinesterase activity was inhibited by ca. 50% in the 2.5 and 5 mg kg−1 groups on either one or both of Days 8 and 15; the liver/body weight ratio increased by 24–79% and the pentobarbital‐induced sleep time decreased by 80–96%. On Days 8 and 15, the in vitro hepatic metabolism of amidopyrine, phenacetin and benzo[a]pyrene in the 2.5 or 5 mg kg−1 group was considerably increased (100–1478%). Findings from this study suggest that these mixtures have the potential to induce the xenobiotic‐metabolizing enzymes in liver; thus, exposures to the pesticidal mixtures might cause deleterious effects in other species, including humans, by enhancing the metabolism of xenobiotics.
Distribution of benzo[a]pyrene in pregnant rats following inhalation exposure and a comparison with similar data obtained with pyrene
Authors: Withey J. R. , Shedden J. , Law F. C. P. , Abedini S. 
Published: October 2006

AbstractEight pregnant rats were exposed, on the 17th day of gestation, for 95 min to a microcondensation aerosol of benzo[a]pyrene at five different atmospheric concentrations between 200 and 800 mg m−3 in a ‘head‐only’ inhalation chamber. Five rats were killed immediately following the exposure and three were killed at 6 h post‐dosing. Concentrations of the radiolabel and ‘free’ benzo[a]pyrene were measured in the individual fetuses and in the maternal blood, fat, kidney, liver and lung.Distribution to the fetus did not appear to be related to its position on the uterine horn and the uptake of benzo[a]pyrene was non‐linear with increasing exposure concentrations, which was similar to the observations previously reported for pyrene. The levels of benzo[a]pyrene were much higher in the fetus and, especially, the lung than those observed in the pyrene study; so also were the levels of total metabolites in these tissues, which might, in part, account for the carcinogenic potency of benzo[a]pyrene.
Organ cadmium deposits in orally exposed female rats and their pups and the depleting efficiency of sodium N‐(4‐methoxybenzyl)‐D‐glucamine‐N‐carbodithioate monohydrate (MeOBDCG)
Authors: Kostial K. , Blanuša M. , Schönwald N. , Arežina R. , Piasek M. , Jones M. M. , Singh P. K. 
Published: October 2006

AbstractCadmium was given to female rats in the drinking water (50 ppm Cd) from 4 weeks before mating until weaning (a total of 10 weeks). Four weeks after the discontinuation of exposure, mothers and offspring were then given two i.p. doses of 1 mmol kg−1 sodium N‐(4‐methoxybenzyl)‐D‐glucamine‐N‐carbodithioate monohydrate (MeOBDCG) on subsequent days. Cadmium in kidneys and liver was determined in groups of mothers before mating and in mothers and pups after parturition, at the end of lactation and 4 and 5 weeks after the discontinuation of exposure. An additional measurement was made in pups in the middle of the lactation. period. Cadmium deposition rapidly increased in the two organs between the 11th and 21st day of lactation. At all times, Cd concentrations in the liver and kidneys of mothers were several orders higher than in the offspring. After the discontinuation of exposure, maternal hepatic and renal Cd contents showed a significant decrease. Treatment with the chelator depleted the hepatic Cd stores in mothers by 90% and in pups by 80%, while the corresponding renal depletions were only 23% and 12%, respectively. The liver and kidney contents of Cd (but not the concentration) increased by a higher factor during lactation than during pregnancy and exposure during lactation was also more important for pups than prenatal exposure.The lower efficiency of the chelator in the offspring indicates that Cd accumulated during the neonatal period was less accessible to treatment with chelating agents than Cd accumulated in later life. It is more likely that with increasing Cd concentration a smaller proportion of Cd is bound to strong binding sites.