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PubMed2006

Effects of exposure time and co-existing organic compounds on uptake of atrazine from nutrient solution by rice seedlings (Oryza sativa L.).

Root uptake of atrazine (ATR) by rice seedlings (Oryza sativa L.) from nutrient solution was investigated with exposure periods of 48, 96, and 240h. A similar ATR uptake was carried out with two co-existing organic compounds (o-chlorophenol (CP) and 2,4-dichlorophenol (DCP)) with 48h exposure. In contact with the seedlings, the ATR level in nutrient solution decreased sharply during the early exposure and then reached relatively steady levels after 48h. It was observed that the ATR levels within whole seedlings approached the estimated equilibrium partition limits in about 48h, according to the partition-limited model utilizing the measured plant water and organic matter contents and the ATR partition coefficients with whole seedlings. However, when roots and shoots were consisted separately, the detected ATR levels in roots were lower than estimated equilibrium limit while the levels in shoots exceeded the equilibrium limit. The data with roots suggested the occurrence of rapid ATR degradation in roots. The results with shoots are intrinsically consistent with the suggested complex formation of ATR with free metal ions in shoots. The ATR levels in roots and shoots varied to a moderate extent when the seedlings were exposed to different levels of ATR-CP-DCP mixtures. The variation results presumably from the interference of coexisting CP and DCP and the phytotoxicity of the mixed chemicals.

Atrazine↗
PubMed2004

Atrazine is a competitive inhibitor of phosphodiesterase but does not affect the estrogen receptor.

Atrazine (ATR), 2-chloro-4-ethylamino-6-isopropylamino-s-triazine, has been implicated in numerous studies to act as an endocrine disruptor, specifically by altering estradiol signaling via increased aromatase activity. Fluorescence polarization (FP) was used to show that the binding equilibria between estrogen receptor-alpha or estrogen receptor-beta, and estradiol were not affected by ATR and its metabolites: ATR-desethyl (ADE), ATR-desisopropyl (ADI), ATR-desethyldesisopropyl (ADD) and terbuthylazine (TBZ). Therefore, ATR and its degradation products were studied to determine their ability to inhibit phosphodiesterase (PDE), the enzyme responsible for hydrolyzing the second messenger cAMP to 5'-AMP. Using FP, it was found that ATR inhibited PDE with an IC50 value of 1.8 microM. This was lower than the known PDE inhibitor isobutyl methylxanthine (IBMX), which had an IC50 value of 4.6 microM. The ATR degradation products ADE, ADI, ADD and TBZ were less effective than ATR at inhibiting PDE when assayed using FP. Classical competitive binding assays, using radiolabeled 14C-cAMP in conjunction with thin layer chromatography (TLC), were used to determine that ATR was a competitive inhibitor of PDE with an association constant of 85 microM.

Atrazine↗
PubMed1988

Photic modulation of a highly sensitive, near-infrared light-scattering signal recorded from intact retinal photoreceptors.

On stimulation by green flashes, the isolated, aspartate-treated bovine retina exhibits transient changes in the scattering of near-infrared (880 nm) light. A single component, termed the "ATR" (a flash-induced scattering signal, where ATR designates amplified transient-retina), dominates the amplitude and rising-phase kinetics of the initial peak of the light-scattering response. Superfusion with physiological solution containing low Na+ concentration reversibly abolishes the photoreceptor electroretinographic response but preserves the ATR signal, indicating a receptoral origin for the ATR. The increase of ATR amplitude (A/Amax) with flash intensity (R*/R, where R indicates rhodopsin) is described by A/Amax = (1- e-kR*/R), with R*/R = k-1 occurring on generation of approximately two photoactivated rhodopsins (R*s) per disc surface in the rod outer segment. Weak background light and bright flashes reversibly depress the ATR. Kinetic and sensitivity data suggest a basis of the ATR in stochastic, unit activation events, each initiated by a single R*. They further suggest an essential invariance of the unit event under differing conditions of illumination. A delay, apparently governed by the lifetime of a light-activated substance regulating ATR generation, precedes ATR recovery after a bright flash. The flash dependence of the delay period indicates an upper limit of 3 s for the lifetime of R* in the ATR-generating process. The unit event appears to be an R*-catalyzed and disc-localized reaction of phototransduction.

Animals↗
PubMed2003

Identification of the human and bovine ATP:Cob(I)alamin adenosyltransferase cDNAs based on complementation of a bacterial mutant.

In humans, deficiencies in coenzyme B12-dependent methylmalonyl-CoA mutase (MCM) lead to methylmalonyl aciduria, a rare disease that is often fatal in newborns. Such deficiencies can result from inborn errors in the MCM structural gene or from mutations that impair the assimilation of dietary cobalamins into coenzyme B12 (Ado-B12), the required cofactor for MCM. ATP:cob(I)alamin adenosyltransferase (ATR) catalyzes the terminal step in the conversion of cobalamins into Ado-B12. Substantial evidence indicates that inherited defects in this enzyme lead to methylmalonyl aciduria, but the corresponding ATR gene has not been identified. Here we report the identification of the bovine and human ATR cDNAs as well as the corresponding human gene. A bovine liver cDNA expression library was screened for clones that complemented an ATR-deficient bacterial strain for color formation on aldehyde indicator medium, and four positive clones were isolated. The DNA sequences of two clones were determined and found to be identical. Sequence similarity searching was then used to identify a homologous human cDNA (89% identity) and its corresponding gene that is located on chromosome XII. The bovine and human cDNAs were independently cloned and expressed in Escherichia coli. Enzyme assays showed that expression strains produced 87 and 98 nmol/min/mg ATR activity, respectively. These specific activities are in line with values reported previously for bacterial ATR enzymes. Subsequent studies showed that the human cDNA clone complemented an ATR-deficient bacterial mutant for Ado-B12-dependent growth on 1,2-propanediol. This demonstrated that the human ATR is active under physiological conditions albeit in a heterologous host. In addition, Western blots were used to show that ATR expression is altered in cell lines derived from cblB methylmalonyl aciduria patients compared with cell lines from normal individuals. We propose that inborn errors in the human ATR gene identified here result in methylmalonyl aciduria. The identification of genes involved in this disorder will allow improvements in the diagnosis and treatment of this serious disease.

Adenosine Triphosphate↗
PubMed1999

Maternal exposure to atrazine during lactation suppresses suckling-induced prolactin release and results in prostatitis in the adult offspring.

The availability of prolactin (PRL) to the neonatal brain is known to affect the development of the tuberoinfundibular (TIDA) neurons and, as a consequence, lead to alterations in subsequent PRL regulation. Without early lactational exposure to PRL (derived from the dam's milk), TIDA neuronal growth is impaired and elevated PRL levels are present in the prepubertal male. These observations, combined with the finding that alterations in PRL secretion (i.e., hyperprolactinemia) in the adult male rat have been implicated in the development of prostatitis, led us to hypothesize that early lactational exposure to agents that suppress suckling-induced PRL release would lead to a disruption in TIDA development, altered PRL regulation, and subsequent prostatitis in the male offspring. To test this hypothesis, suckling-induced PRL release was measured in Wistar dams treated twice daily with the herbicide atrazine (ATR, by gavage, on PND 1-4 at 0, 6.25, 12.5, 25, and 50 mg/kg body weight), or twice daily with the dopamine receptor agonist bromocriptine (BROM, sc, at 0.052, 0.104, 0.208, and 0.417 mg/kg); BROM is known to suppress PRL release. Similarly, atrazine has also been reported to suppress PRL in adult females. Serum PRL was measured on PND 3 using a serial sampling technique and indwelling cardiac catheters. A significant rise in serum PRL release was noted in all control females within 10 min of the initiation of suckling. Fifty-mg/kg ATR inhibited suckling-induced PRL release in all females, whereas 25 and 12.5 mg/kg ATR inhibited this measure in some dams and had no discernible effect in others. The 6.25 mg/kg dose of ATR was without effect. BROM, used here as a positive control, also inhibited suckling-induced PRL release at doses of 0.104 to 0.417 mg/kg, with no effect at 0.052 mg/kg. To examine the effect of postnatal ATR and BROM on the incidence and severity of inflammation (INF) of the lateral prostate of the offspring, adult males were examined at 90 and 120 days. While no effect was noted at 90 days of age, at 120 days, both the incidence and severity of prostate inflammation was increased in those offspring of ATR-treated dams (25 and 50 mg/kg). The 12.5 mg/kg ATR and the two highest doses of BROM increased the incidence, but not the severity, of prostatitis. Combined treatment of ovine prolactin (oPRL) and 25 or 50 mg/kg ATR on PND 1-4 reduced the incidence of inflammation observed at 120 days, indicating that this increase in INF, seen after ATR alone, resulted from the suppression of PRL in the dam. To determine whether or not there is a critical period for these effects, dams were dosed with 25 and 50 mg/kg on PND 6-9 and PND 11-14. Inflammation was increased in those offspring from dams treated on PND 6-9, but this increase was not significant. Dosing on PND 11-14 was without effect. These data demonstrate that ATR suppresses suckling-induced PRL release and that this suppression results in lateral prostate inflammation in the offspring. The critical period for this effect is PND 1-9.

Animals↗
PubMed1994

Two distinct transmembrane serine/threonine kinases from Drosophila melanogaster form an activin receptor complex.

A transmembrane protein serine/threonine kinase, Atr-I, that is structurally related to receptors for members of the transforming growth factor-beta (TGF-beta) family has been cloned from Drosophila melanogaster. The spacing of extracellular cysteines and the cytoplasmic domain of Atr-I resemble most closely those of the recently described mammalian type I receptors for TGF-beta and activin. When expressed alone in test cells, Atr-I is unable to bind TGF-beta, activin, or bone morphogenetic protein 2. However, Atr-I binds activin efficiently when coexpressed with the distantly related Drosophila activin receptor Atr-II, with which it forms a heteromeric complex. Atr-I can also bind activin in concert with mammalian activin type II receptors. Two alternative forms of Atr-I have been identified that differ in an ectodomain region encompassing the cysteine box motif characteristic of receptors in this family. Comparison of Atr-I with other type I receptors reveals the presence of a characteristic 30-amino-acid domain immediately upstream of the kinase region in all these receptors. This domain, of unknown function, contains a repeated Gly-Ser sequence and is therefore referred to as the GS domain. Maternal Atr-I transcripts are abundant in the oocyte and widespread during embryo development and in the imaginal discs of the larva. The structural properties, binding specificity, and dependence on type II receptors define Atr-I as an activin type I receptor from D. melanogaster. These results indicate that the heteromeric kinase structure is a general feature of this receptor family.

Activin Receptors↗
PubMed1981

Peripheral and central effects of atropine and chlorpromazine on gastric motility and ulceration in stressed rats.

In rats exposed to restraint and water immersion stress, inhibitory effects of atropine (ATR) and chlorpromazine (CPZ) on stress-induced gastric ulceration and motility were studied to clarify which of central and peripheral origins was responsible for these effects. The drug dose ratio of peripheral (intravenous, i.v.) route versus central (intracerebroventricular, i.c.v.) route required to produce an approx. 50% inhibition of gastric ulceration or motility was estimated. Gastric ulceration was prevented by pretreatment with each drug via either route, and there was no great difference in the dose ratio of each drug (i.v.:i.c.v. = 4:1) for the inhibition. The stress-enhanced gastric motility was immediately depressed by each drug via either route. This inhibitory effect of CPZ was short-lasting as compared with that of ATR, and the complete blockade was observed after administration of i.v. ATR or i.c.v. CPZ at higher doses. The ATR dose ratio for this inhibition was less than 10, while the CPZ dose ratio was from 10 to 25. The treatment with CPZ, but not with ATR, caused a definite change in EEG patterns, along with a decrease in body temperature or heart rate. The effect of pretreatment with ATR or CPZ on gastric motility during stress was also investigated. Only the administration of ATR, via either route, appreciably inhibited the gastric motility. Thus, it was suggested that: (1) the inhibitory effect of ATR on gastric motility may be of peripheral rather than central origin, while that of CPZ predominantly of central origin; (2) the anti-ulcerogenic effect of ATR and CPZ may be predominantly of peripheral origin, and the mechanisms involved in ATR may be associated with inhibition of gastric motility, which is different from those in CPZ.

Animals↗
PubMed2002

The effects of atrazine on the sexual maturation of female rats.

The mammalian hazard assessment of the herbicide atrazine (ATR) has focused on the induction of mammary tumors and accelerated reproductive aging of adult rats, and the relationship of these effects to the inhibition of leutinizing hormone (LH) release from the pituitary, an effect itself caused by inhibition of GnRH signaling by the adult rat hypothalamus. In earlier studies, Laws et al. (Toxicol. Sci., 58, 366-376, 2000) demonstrated a delay in female rat sexual maturation induced by ATR, effects that could equally have been caused by inhibition of hypothalamic GnRH release. The present studies were designed to compare the doses that interfere with GnRH signaling seen in previous studies in adult Sprague-Dawley (SD) rats (LH surge suppression) with doses that impair GnRH signaling in peripubertal rats, as indicated by delayed sexual maturation. The studies evaluated the effects of ATR treatment on the timing of uterine growth and vaginal opening (VO) in peripubertal female Wistar (Alderley Park, AP) and SD rats. Doses of 10, 30, and 100 mg/kg ATR were administered daily from postnatal day (pnd) 21 to up to pnd 46. Determinations of uterine weight were made at pnd 30, 33, 43 (AP), and 46 (SD) and the timing of VO was also assessed in the last two of these experiments. The centrally acting GnRH antagonist Antarelix (ANT) was used as a positive control agent as it has previously been shown to prevent uterine growth and to delay VO in peripubertal AP rats. Uterine growth and VO were completely prevented in AP rats exposed to ANT. Uterine growth was delayed at pnd 30 and 33 in AP rats exposed to 100 mg/kg ATR, but this growth inhibition had been overcome by pnd 43. VO was significantly delayed in AP rats for the 100 mg/kg ATR dose. By pnd 46, VO was significantly delayed in SD rats exposed to both 30 and 100 mg/kg ATR, but uterine weights were unaffected by that time (as for AP rats). It is concluded that the no-effect level for the effects of ATR on sexually immature rats (10 mg/kg in SD; 30 mg/kg AP) is approximately the same as reported previously by Laws et al. in peripubertal Wistar rats (25 mg/kg). However, the no-effect level in peripubertal female SD rats is nearly an order of magnitude greater than the no-observed effect level observed in female SD rats fed ATR for 6 months (1.8 mg/kg) where LH suppression was used as an indicator of effect on the pituitary/hypothalamic axis (USEPA, Atrazine-DACT Fourth Report of the Hazard Identification and Review Committee, April 5, 2002). These results support the conclusion that the pituitary/hypothalamic axis in peripubertal female SD rats is less sensitive than that in adult female SD rats.

Administration, Oral↗
PubMed1983

Synthesis and properties of fluorescent derivatives of atractyloside as potential probes of the mitochondrial ADP/ATP carrier protein.

The chemical synthesis of fluorescent derivatives of atractyloside (ATR), an inhibitor of the mitochondrial ADP/ATP carrier protein, is described. These derivatives are the following: 6'-O-dansyl ATR, 6'-O-dansyl-aminobutyryl ATR, and 6'-O-naphthoyl ATR. The spectral properties of these analogs were analyzed, and their biological features were compared to those of ATR. The fluorescence emission of the dansyl ATR derivatives was increased in organic solvents and that of naphthoyl ATR was decreased; for both analogs, solubilization in organic solvents resulted in a blue shift of the emission peak. The fluorescent dansyl and naphthoyl ATR derivatives were specifically recognized by the mitochondrial ADP/ATP carrier protein. Because of their spectral properties and their biochemical reactivities, the fluorescent analogs of ATR can be considered as potential probes to investigate the topography of the ADP/ATP carrier in the mitochondrial membrane and to monitor conformational changes of the ADP/ATP carrier protein associated with transport.

Adenosine Diphosphate↗
PubMed2000

Effect of atrazine on implantation and early pregnancy in 4 strains of rats.

Atrazine (ATR) is an herbicide that has been shown to have adverse reproductive effects including alterations in levels of pituitary hormones such as prolactin (prl) and luteinizing hormone (LH) in female LE rats when administered at doses of 200 mg/kg/day for 1 and 3 days. Because the action of prl in promotion of progesterone secretion is essential for the initiation of pregnancy in rats, this study was designed to examine the effect of exposure to ATR during early pregnancy on implantation and short-term pregnancy maintenance. Rats were divided into two groups representing periods of dosing with ATR prior to the diurnal or nocturnal surges of prl. Within each group, four groups consisting of four strains of rats [Holtzman (HLZ); Sprague Dawley (SD); Long Evans (LE); Fischer 344 (F344)] were each further subdivided into four ATR dosages. Rats were dosed by gavage with 0, 50, 100, or 200 mg/kg/day ATR on days 1-8 of pregnancy (day 0 = sperm +). All animals were necropsied on day 8 or 9 of pregnancy. The 200 mg/kg dose of ATR reduced body weight gain in all but one group. Two groups of animals dosed at 100 and 200 mg/kg/day in the nocturnal dosing period showed an increase in percent preimplantation loss, and both of these were F344 rats. HLZ rats were the only strain to show a significant level of postimplantation loss and a decrease in serum progesterone at 200 mg/kg/day both following diurnal and nocturnal dosing. Doses of 100 mg/kg/day also produced postimplantation loss following diurnal and nocturnal dosing, but progesterone levels were decreased only after nocturnal dosing. Alterations in serum LH were seen in several groups. Serum estradiol was significantly increased only in SD rats dosed at the diurnal interval with 200 mg/kg ATR. We conclude that F344 rats are most susceptible to preimplantation effects of ATR and that HLZ rats appear most sensitive to the postimplantation effects of the chemical. LE and SD rats were least sensitive to effects of ATR during very early pregnancy.

Administration, Oral↗
PubMed1997

Long-term renal allograft survival: prognostic implication of the timing of acute rejection episodes.

BACKGROUND: The timing of an acute rejection may have a variable impact on renal allograft survival. To determine whether the time of first acute transplant rejection (ATR) is an independent predictor of long-term allograft survival, we studied 31,600 first cadaveric renal transplants that were functional on the first transplant anniversary, from 217 U.S. centers. METHODS: Transplant patients were divided into four groups according to the time to the first ATR: no rejection in year 1 (group I); predischarge ATR (group II); first ATR between discharge and month 6 (group III); and first ATR in months 7-12 (group IV). RESULTS: Four-year allograft survival after year 1, estimated by a Cox proportional hazard model adjusting for 19 cofactors, was 78%, 72%, 69%, and 54% for groups I-IV, respectively (P<0.0001 for each comparison to group I). In those patients who had ATR episodes in more than one time period, later episodes were associated with worse long-term allograft survival, an observation that was independent of previous ATR episodes. CONCLUSIONS: We conclude that late occurrence of a first acute rejection portends a worse prognosis for allograft survival after the first year. Later rejections, in combination with previous rejections, also lead to worse long-term allograft survival. Unlike early ATRs occurring in the setting of supervised immunosuppression, late occurring ATR may reflect inadequate immunosuppression from noncompliant behavior or may reflect disruption or lack of immune tolerance to the allograft. Efforts to minimize late transplant loss require a combination of strategies directed at both immunologic and behavioral factors.

Acute Disease↗
PubMed1980

Effects of timepidium bromide, hyoscine-N-butylbromide and atropine on the isolated guinea pig gallbladder and sphincter of Oddi.

Effects of timepidium bromide (TB), hyoscine-N-butylbromide (HB) and atropine (Atr) were studied on the isolated guinea pig gallbladder and sphincter of Oddi. In the isolated gallbladder, the contraction induced by methacholine was competitively antagonized with TB, HB and Atr: pA2 values for TB, HB and Atr were 8.44, 7.55 and 9.11, respectively. Contraction of gallbladder after field stimulation at 5 Hz was also inhibited by TB, HB and Atr as well as by tetrodotoxin (TTX). On the other hand, TB had no significant influence on the electrically evoked (30 Hz) contraction which remained after treatment with TTX. It was estimated that the inhibitory activity of TB on the contraction of gallbladder was 1/5-1/6 that of Atr and 7 times as potent as HB. In the isolated sphincter of Oddi, TB, HB and Atr reduced the perfusion pressure increased by acetylcholine (ACh), the activity of TB being 1/4 that of Atr and 3 times of HB. The contractile responses to field stimulation (5 Hz) were also inhibited by TB, HB and Atr. The inhibitory activity of TB was 1/5 that of Atr and 12 times of HB. It was also demonstrated that TB produced no significant effect on the noradrenaline (Nor)-induced contraction and isoproterenol (Iso)-induced relaxation in the gallbladder or Nor-induced increase of the perfusion pressure in the sphincter of Oddi. It is suggested that TB acts on the gallbladder and sphincter of Oddi by virtue of its anticholinergic activity.

Acetylcholine↗
PubMedDate not supplied

Dose-response effects of atropine and HI-6 treatment of organophosphorus poisoning in guinea pigs.

HI-6 (1-2-hydroxyiminomethyl-1-pyridino-3-(4-carbamoyl-1-pyridino -2- oxapropane dichloride) has been evaluated as an oxime alternative to pralidoxime, and toxogonin in the treatment of organophosphorus (OP) poisoning. The dose response effects of atropine (ATR) and HI-6 were investigated to more fully explore the interaction of these compounds in the treatment of OP poisoning. ATR, HI-6 and various combinations of the two drugs were evaluated against lethal poisoning by soman (GD) and tabun (GA) in guinea pigs. The effect of adjunctive diazepam treatment on the efficacy of atropine and HI-6 against soman was also investigated. Animals of either sex were challenged s.c. with OP and treated i.m. 1 min later with ATR and/or HI-6. When used, diazepam was injected immediately after ATR+HI6. LD50s of each treatment were calculated from probit models based on 24-hour survival against 5 levels of nerve agent and 6 animals per challenge level. A protective index (PI) was calculated by dividing the nerve agent LD50 in the presence of treatment by the LD50 in the absence of treatment. Treatment with HI6 alone had little effect on the toxicity of either OP. Treatment with ATR alone was more effective than HI-6 alone and was significantly more effective against soman than against tabun. When used in combination atropine and HI-6 had a strong synergistic effect against both agents. The dose of atropine used with HI-6 was critical in determining the efficacy of HI-6 against either agent. The slopes of the dose-lethality curves were minimally affected by the dose of ATR or HI-6. Adjunctive treatment with diazepam enhanced the efficacy of HI-6 and atropine against soman. It is concluded that 1) ATR has a large effect on the efficacy of HI-6 against OP poisoning, 2) the dose of ATR must be carefully selected in studies investigating the efficacy of HI-6 against OP poisoning, 3) the effective dose of ATR in the guinea pig is approximately 16 mg/kg, and 4) diazepam is a useful adjunct to atropine and HI-6.

Animals↗
PubMed1993

[The action of atracurium and vecuronium in chronically hemodialyzed patients].

UNLABELLED: Reports on the duration of action of atracurium (Atr) and vecuronium (Vec) in patients with renal failure are contradictory. It is either stated that the duration is equal for both relaxants or that Atr acts for a longer duration. Because of these conflicting results, we measured the times for latency (tL), onset (tA), duration of action (tW), and recovery (tE) for both agents. METHODS: Fourty patients with end-stage renal failure on chronic haemodialysis were randomly assigned to receive either Atr (0.4 mg.kg-1 BW) or Vec (0.08 mg.kg-1 BW). After induction with thiopentone and 0.1 mg fentanyl, anaesthesia was maintained with nitrous oxide and 1 vol.% ethrane and expiratory CO2 partial pressure was kept between 4.6 and 4.9 kPa. If the twitch height of T1 regained 25% of the pre-relaxation value, 20% of the initial relaxant bolus was injected. Relaxation was monitored with a relaxograph after calibration of the device. After testing for a normal distribution, statistical analysis was done by Student's t-test. A value of P < or = 0.05 was chosen for statistical significance. RESULTS: There were no significant differences regarding tL (Atr: 1.0 +/- 0.5 min; Vec: 1.1 +/- 0.5 min) and tA (Atr: 5.5 +/- 2.1 min; Vec 4.1 +/- 2.4 min); tW (Atr: 21.3 +/- 13.1 min; Vec 31.7 +/- 15.6 min) and tE (Atr: 19.0 +/- 9.0 min; Vec 30.1 +/- 19.0) were significantly different. DISCUSSION: Our results are not in accordance with those authors who found in comparison with Atr an equal or shorter duration of action for Vec in patients with renal failure. If the duration of action is equal in subjects with no renal insufficiency, our measurements are in accordance with kinetic evaluations showing the same clearance and half-life for Atr in patients with and without renal insufficiency, but 40% diminished clearance and 60% prolonged half-life for Vec in renal insufficiency.

Adult↗
PubMed1993

[Effects of atropine on contraction of rabbit aortic smooth muscle and cell proliferation].

The calcium antagonistic actions of atropine (Atr) and verapamil (Ver) were studied on the contraction of rabbit thoracic aorta strips induced by CaCl2 and KCl. Both Atr and Ver were found to depress the contraction as demonstrated by the shift-to-right of the dose-effect relationship curves and the decrease of maximal responses, with the value of pD'2 being 4.4 and 5.8 respectively. The intracellular Ca(2+)-dependent component of NE-induced aortic strip contraction was also inhibited by the 2 drugs, but the extracellular Ca(2+)-dependent component was barely or not inhibited by Atr before its concentration was raised to 100 mumol/L. These results indicate that the depressive effect of Atr on aortic contraction is mainly exerted by acting on the PDC (potential-dependent channel). The action of Atr on proliferation of cells was also studied in rabbit aortic smooth muscle cell (ASMC) culture. The growth was inhibited by Atr when Ca2+ was present in the medium. When Ca2+ was absent, however, the growth was stimulated by Atr 20.6-185.2 mumol/L, but inhibited by Atr 555.7-1666.7 mumol/L, suggesting that Ca2+ is somehow involved in the action of Atr on ASMC growth.

Animals↗
PubMed2006

Achilles tendon rupture and its association with fluoroquinolone antibiotics and other potential risk factors in a managed care population.

BACKGROUND: Case reports and observational studies have implicated fluoroquinolone antibiotic exposure as a risk factor for Achilles tendon rupture (ATR), an uncommon condition for which there are few formal studies. We sought to quantify the strength of association between exposure to fluoroquinolone antibiotics and the occurrence of ATR, accounting for other risk factors. METHODS: This was a case-control study nested within a health insurer cohort. Cases of ATR were identified and confirmed using patterns of health insurance claims that were validated through sampled medical record review. Information on risk factors, including fluoroquinolone exposure, came from health insurance claims. RESULTS: There were 947 cases of ATR and 18 940 controls. A dispensing of a fluoroquinolone antibiotic in the past 6 months was more common among ATR cases than controls, although not significantly so (odds ratio (OR) = 1.2; 95% confidence interval (CI) = 0.9-1.7), and exposure to a higher cumulative fluoroquinolone dose was more strongly associated (OR = 1.5, 95%CI = 1.0-2.3). Other risk factors for ATR were trauma (OR = 17.2, 95%CI = 14.0-20.2), male sex (OR = 3.0, 95%CI = 2.6-3.5), injected corticosteroid administration (OR = 2.2, 95%CI = 1.6-2.9), obesity (OR = 2.0, 95%CI = 1.2-3.1), rheumatoid arthritis (OR = 1.9, 95%CI = 1.0-3.7), skin or soft tissue infections (OR = 1.5, 95%CI = 0.9-2.3), oral corticosteroids (OR = 1.4, 95%CI = 1.0-1.8), and non-fluoroquinolone antibiotics (OR = 1.2, 95%CI = 1.1-1.5). CONCLUSIONS: The elevation in ATR risk associated with fluoroquinolones was similar in magnitude to that associated with oral corticosteroids or non-fluoroquinolone antibiotics. Trauma and male sex were more strongly associated with ATR, as were obesity and injected corticosteroids.

Achilles Tendon↗
PubMed2006

The amplitude of the Achilles tendon reflex in infants is related to body position.

In this study, we investigated whether the Achilles tendon reflex (ATR) in healthy infants is modulated by changes in body position (prone vs. supine). The amplitude of the ATR was compared at postnatal day 1, months 2, 3 and 6, while infants were placed in prone and supine position. The ATR was considered "positive" when at least 1 of 20 tendon taps evoked a visible contraction of the ankle plantar flexor muscles. At 6 months, the amplitude and latency of the ATR were evaluated by electromyographic (EMG) recordings of the (lateral and medial) gastrocnemius muscle, with the infant in prone and supine position. At postnatal day 1, the clinical ATR response was more frequently present in prone than supine position (14/16 or 88% vs. 4/16 or 25%, respectively, p < 0.01). From 2 months onwards, the frequencies of positive ATRs were no longer significantly different between prone (14/14 or 100%) and supine position (10/14 or 67%). However, based on the EMG recordings at 6 months, the ATR amplitude was higher in prone compared to supine position (n=8, median 5.5 mV, range 4.7-6.6 mV; and median 3.8 mV, range 2.3-5.6 mV, p < 0.05). We conclude that the ATR response in healthy infants is more pronounced in prone than in supine position, either when clinically (visually) assessed during routine tendon tapping or when neurophysiologically assessed during surface EMG recording.

Achilles Tendon↗
PubMed2006

Cytosolic and localized inhibition of phosphodiesterase by atrazine in swine tissue homogenates.

Atrazine (ATR) significantly inhibited phosphodiesterase (PDE) in crude homogenates of swine heart, brain, and lung, but not liver or kidney tissues. Except for heart, PDE activities in the cytosolic fraction of the tissue homogenates were not affected by ATR. The inhibition of the PDE activity in the cytosol from heart homogenate was not significantly different between ATR and a non-specific PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX). Dixon plots of the crude tissue homogenates showed that heart and brain were inhibited via two different mechanisms (competitive or mixed inhibition, and noncompetitive inhibition, respectively), suggesting that ATR may be a semi-specific PDE inhibitor. Furthermore, in crude tissue homogenates, ATR did not inhibit PDE as effectively as IBMX suggesting that there are ATR-susceptible and ATR-nonsusceptible forms of PDE. Association constants for ATR were 55 microM for heart and 310 microM for brain. The stability of the activity of PDE was affected by freezing, requiring the use of only freshly prepared tissue homogenates.

1-Methyl-3-isobutylxanthine↗