scholarly journals Renal epoxyeicosatrienoic acid synthesis during pregnancy

2005 ◽  
Vol 288 (1) ◽  
pp. F221-F226 ◽  
Author(s):  
Yiqiang Zhou ◽  
Hsin-Hsin Chang ◽  
Juan Du ◽  
Cong-Yi Wang ◽  
Zheng Dong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Immunohistochemical Analysis ◽  
Acid Synthesis ◽  
The Body ◽  
Female Rats ◽  
Epoxyeicosatrienoic Acid ◽  
Pregnant Rats ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Renal Tubular

Epoxyeicosatrienoic acids (EETs), which belong to cytochrome P-450 (CYP)-derived eicosanoids, have been implicated to vasodilate renal arterioles, inhibit sodium transport in the nephron, and regulate blood pressure in several animal models. Because pregnancy is associated with changes of blood pressure, the aim of this study was to examine whether renal EET synthesis is altered and whether EETs are involved in blood pressure regulation during pregnancy in rats. Renal microsomal epoxygenase activity increased by 47, 97, and 63% on days 6, 12, and 19 of gestation, respectively. The elevation of epoxygenase activity during pregnancy was associated with an increase in CYP2C11, CYP2C23, and CYP2J2 protein expression on days 6, 12, and 19 of gestation. Moreover, immunohistochemical analysis showed that renal tubular CYP2C11, CYP2C23, and CYP2J2 expression was significantly increased in pregnant rats on days 6, 12, and 19 of gestation. Administration of 6-(2-propargyloxyphenyl)hexanoic acid (PPOH), a selective epoxygenase inhibitor, caused a dose-dependent inhibition of microsomal expoxygenase activity without a significant effect on ω-hydroxylase activity in female rats. Interestingly, administration of PPOH (20 mg·kg−1·day−1 for 4 days starting on day 15 of pregnancy) increased blood pressure by 21 mmHg and caused a significant decrease in the body weight of fetal pups (1.3 ± 0.08 g in control vs. 1.1 ± 0.06 g in PPOH). Moreover, PPOH treatment significantly decreased renal microsomal epoxygenase activity and the expression of CYP2C11, CYP2C23, and CYP2J in pregnant rats. This study demonstrates that EET synthesis in the kidney is elevated during pregnancy, and CYP2C11, 2C23, and CYP2J2 are responsible for the change of renal EET synthesis. The inhibition results demonstrate that the downregulation of renal epoxygenase activity by PPOH causes hypertension in pregnant rats. This study suggests that EETs may contribute to the control of blood pressure during pregnancy.

Regulation of renal CYP4A expression and 20-HETE synthesis by nitric oxide in pregnant rats

2003 ◽  
Vol 285 (2) ◽  
pp. F295-F302 ◽  
Author(s):  
Mong-Heng Wang ◽  
Jishi Wang ◽  
Hsin-Hsin Chang ◽  
Barbara A. Zand ◽  
Miao Jiang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Rat Kidney ◽  
Late Pregnancy ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Male Rats ◽  
Pregnant Rats ◽  
Renal Vasoconstriction ◽  
Dependent Inhibition

20-Hydroxyeicosatetraenoic acid (20-HETE), which promotes renal vasoconstriction, is formed in the rat kidney primarily by cytochrome P-450 (CYP) 4A isoforms (4A1, 4A2, 4A3, 4A8). Nitric oxide (NO) has been shown to bind to the heme moiety of the CYP4A2 protein and to inhibit 20-HETE synthesis in renal arterioles of male rats. However, it is not known whether NO interacts with and affects the activity of CYP4A1 and CYP4A3, the major renal CYP4A isoforms in female rats. Incubation of recombinant CYP4A1 and 4A3 proteins with sodium nitroprusside (SNP) shifted the absorbance at 440 nm, indicating the formation of a ferric-nitrosyl-CYP4A complex. The absorbance for CYP4A3 was about twofold higher than that of CYP4A1. Incubation of SNP or peroxynitrite (PN; 0.01–1 mM) with CYP4A recombinant membranes caused a concentration-dependent inhibition of 20-HETE synthesis, with both chemicals having a greater inhibitory effect on CYP4A3-catalyzed activity. Moreover, incubation of CYP4A1 and 4A3 proteins with PN (1 mM) resulted in nitration of tyrosine residues in both proteins. In addition, PN and SNP inhibited 20-HETE synthesis in renal microvessels from female rats by 65 and 59%, respectively. We previously showed that microvessel CYP4A1/CYP4A3 expression and 20-HETE synthesis are decreased in late pregnancy. Therefore, we investigated whether such a decrease is dependent on NO, the synthesis of which has been shown to increase in late pregnancy. Administration of NG-nitro-l-arginine methyl ester (l-NAME) to pregnant rats for 6 days ( days 15- 20 of pregnancy) caused a significant increase in systolic blood pressure, which was prevented by concurrent treatment with the CYP4A inhibitor 1-aminobenzotriazole (ABT). Urinary NO2/NO3 excretion decreased by 40 and 52% in l-NAME- and l-NAME + ABT-treated groups, respectively. Interestingly, renal microvessel 20-HETE synthesis showed a marked increase following l-NAME treatment, and this increase was diminished with coadministration of ABT. These results demonstrate that NO interacts with CYP4A proteins in a distinct manner and it interferes with renal microvessel 20-HETE synthesis, which may play an important role in the regulation of blood pressure and renal function during pregnancy.

Pharmacodynamics of alacepril in healthy cats

2016 ◽  
Vol 19 (6) ◽  
pp. 706-709
Author(s):  
Keisuke Sugimoto ◽  
Yoko Fujii ◽  
Izumi Takubo ◽  
Toshinori Shiga ◽  
Hiroshi Sunahara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Clinical Use ◽  
Converting Enzyme ◽  
Serum Angiotensin Converting Enzyme ◽  
Blood Samples ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Ace Activity ◽  
Dose Dependent ◽  
Time Point

Objectives The aims of this study were to investigate the pharmacodynamics of alacepril and to determine the appropriate dose for clinical usage in cats. Methods Six experimental cats were used. Each cat received alacepril orally at a single dose of 1 mg/kg, 2 mg/kg and 3 mg/kg. Blood samples were collected before administration and at 2, 4, 6, 8, 12, 24, 36, 48 and 72 h after administration to measure serum angiotensin converting enzyme (ACE) activity. Systolic blood pressure was also measured at the same time point. Results Dose-dependent inhibition of ACE activity was observed. Doses of 2 mg/kg and 3 mg/kg alacepril were considered to effectively inhibit ACE activity. There were no significant differences in systolic blood pressue among groups at any time point. Conclusions and relevance Alacepril 2–3 mg/kg q24h may be an appropriate dosage for clinical use in cats.

scholarly journals Vascular Response to Graded Angiotensin II Infusion in Offspring Subjected to High-Salt Drinking Water during Pregnancy: The Effect of Blood Pressure, Heart Rate, Urine Output, Endothelial Permeability, and Gender

2014 ◽  
Vol 2014 ◽  
pp. 1-8
Author(s):  
Zahra Pezeshki ◽  
Fatemeh Eshraghi-Jazi ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Urine Output ◽  
The Body ◽  
High Salt ◽  
Female Rats ◽  
Kidney Weight ◽  
Group 3

Introduction.Rennin-angiotensin system and salt diet play important roles in blood pressure control. We hypothesized that the high-salt intake during pregnancy influences the degree of angiotensin-dependent control of the blood pressure in adult offspring.Methods.Female Wistar rats in two groups (A and B) were subjected to drink tap and salt water, respectively, during pregnancy. The offspring were divided into four groups as male and female offspring from group A (groups 1 and 2) and from group B (groups 3 and 4). In anesthetized matured offspring mean arterial pressure (MAP), heart rate and urine output were measured in response to angiotensin II (AngII) (0-1000 ng/kg/min, iv) infusion.Results.An increase in MAP was detected in mothers with salt drinking water (P<0.05). The body weight increased and kidney weight decreased significantly in male offspring from group 3 in comparison to group 1 (P<0.05). MAP and urine volume in response to AngII infusion increased in group 3 (P<0.05). These findings were not observed in female rats.Conclusion.Salt overloading during pregnancy had long-term effects on kidney weight and increased sex-dependent response to AngII infusion in offspring (adult) that may reveal the important role of diet during pregnancy in AngII receptors.

scholarly journals Altered vascular contractility in adult female rats with hypertension programmed by prenatal glucocorticoid exposure

2006 ◽  
Vol 188 (3) ◽  
pp. 435-442 ◽  
Author(s):  
P W F Hadoke ◽  
R S Lindsay ◽  
J R Seckl ◽  
B R Walker ◽  
C J Kenyon
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Adult Female ◽  
Vascular Function ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Control Group ◽  
Pregnant Rats ◽  
Vascular Contractility

Excessive exposure to glucocorticoids during gestation reduces birth weight and induces permanent hypertension in adulthood. The mechanisms underlying this programmed elevation of blood pressure have not been established. We hypothesised that prenatal glucocorticoid exposure may lead to vascular dysfunction in adulthood. Pregnant rats received dexamethasone (Dex) (100 μg/kg, s.c.) or vehicle (control) daily throughout pregnancy. Blood pressure was elevated (students t-test, unpaired; P < 0.05) in adult female offspring (aged 12–16 weeks) of Dex-treated mothers (148.0 ± 3.6 mmHg, n=10) compared with the control group (138.0 ± 2.5 mmHg, n=8). Vascular responsiveness in aortae and mesenteric arteries was differentially affected by prenatal Dex: aortae were less responsive to angiotensin II, whereas mesenteric arteries were more responsive to norepinephrine, vasopressin and potassium (mesenteric arteries respond poorly to angiotensin II in vitro). Acetylcholine-mediated, endothelium-dependent relaxation was similar in both groups. Prenatal exposure to Dex had no effect on blood pressure or aldosterone response to acute (15 min, i.v.) infusion of angiotensin II (75 ng/kg per min). In contrast, chronic (2-week, s.c.) infusion of angiotensin II (100 ng/kg per min) produced a greater elevation (P < 0.05) of blood pressure in Dex-treated rats (150.0 ± 3.6 mmHg) than in controls (135.3 ± 5.4 mmHg), and aldosterone levels were higher in Dex-treated animals. There was no angiotensin II-induced medial hypertrophy/hyperplasia in mesenteric arteries from Dex-treated rats. These results indicate that vascular function is altered in a region-specific manner in rats with glucocorticoid-programmed hypertension. Despite a striking increase in mesenteric artery contraction in Dex-treated rats, in vivo studies suggest that abnormalities of the renin-angiotensin-aldosterone system, rather than enhanced vascular contractility, may be responsible for the elevation of blood pressure in these animals.

scholarly journals The Effect of BML-111 in Preeclampsia Rat Model Induced by the Low Dose of Cadmium Chloride

2019 ◽  
Vol 09 (03) ◽  
pp. e201-e208 ◽  
Author(s):  
KeKe Zhang ◽  
Min Hu ◽  
Lin Zhang ◽  
Qiong Zhang ◽  
Yinping Huang
Keyword(s):  
Blood Pressure ◽  
Rat Model ◽  
Cadmium Chloride ◽  
Therapeutic Potential ◽  
The Body ◽  
Optimal Time ◽  
Pregnant Rats ◽  
Multiple Features ◽  
Pregnant Rat ◽  
Messenger Ribonucleic Acid

Aim This article determines the optimal time and dose of cadmium chloride (CdCl2) injected to pregnant rat to establish experimental preeclampsia (PE) model. In addition, the therapeutic potential of BML-111, a lipoxin A4 analogue, in the CdCl2-induced PE model was also evaluated. Methods Peritoneal injection of two dose of CdCl2 for successive 6 days was tested in the pregnant rats starting from various gestational days (GDs). During this process, the systolic blood pressure and the body weight of pregnant rats and neonatal rats were monitored. The pathological changes of the placenta and kidney were evaluated by hematoxylin and eosin staining. The phosphorylation of extracellular signal-regulated kinase 1/2 and signal transducer and activator of transcription 3 in the placentas was detected by Western blot, and the messenger ribonucleic acid expression of interleukin (IL)-6, tumor necrosis factor-α, and IL-10 in the placentas were detected by real-time polymerase chain reaction. BML-111 at the dose of 1 mg/kg/day was peritoneally injected into the rat after establishing the PE model to test its therapeutic potential. Results In the present study, we successfully established the PE model in pregnant rats by intraperitoneally injection of CdCl2 at the dose of 0.125 mg/kg/day from GD 9 to 14. We recapitulated multiple features of clinical PE in CdCl2-induced rat, including high blood pressure, renal dysfunction, and inflammatory response in placenta. Furthermore, treatment with BML-111 significantly relieved multiple features in our PE rat model. Conclusions BML-111 has a potential therapeutic effect in pregnant rats with CdCl2-induced PE, which appears to be mediated through inhibition of inflammatory processes in the placenta.

Uterine Cervical Distension Induces cFos Expression in Deep Dorsal Horn Neurons of the Rat Spinal Cord

2003 ◽  
Vol 99 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Chuanyao Tong ◽  
Weiya Ma ◽  
Sang-Wook Shin ◽  
Robert L. James ◽  
James C. Eisenach
Keyword(s):  
Spinal Cord ◽  
Dorsal Horn ◽  
Inhibitory Effect ◽  
Central Canal ◽  
Labor Pain ◽  
Female Rats ◽  
Dorsal Horn Neurons ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Surgical Preparation

Background Uterine cervical distension underlies labor pain, yet its neurophysiology and pharmacology of inhibition remain unexplored. The authors examined uterine cervical distension-evoked cFos immunoreactivity in rat spinal cords, and the inhibitory effect of spinal cyclo-oxygenase inhibition on cFos expression. Methods Female rats were anesthetized with halothane, and pairs of metal rods were inserted in each cervical os through a mid-line laparotomy. A submaximal distension force (75 g) was applied for either 30 or 60 min, or, in control animals, no force was applied. Other animals received cervical lidocaine infiltration prior to uterine cervical distension. At the end of the experiments, the spinal cord at T12 to L2 levels was harvested and immunostained for cFos protein. Other animals received intrathecal ketorolac (0, 5, 25, and 50 microg; n = 5-6 for each group) prior to uterine cervical distension. Results Uterine cervical distension significantly increased cFos immunoreactivity in the spinal cord from T12 to L2, with most cFos expression in the deep dorsal and central canal regions. Surgical preparation alone without uterine cervical distension resulted in minimal cFos expression, primarily in the superficial dorsal horn. Uterine cervical distension-evoked cFos expression was prevented by prior infiltration of lidocaine into the cervix. Intrathecal ketorolac produced a dose-dependent inhibition of uterine cervical distension-induced cFos expression. Conclusion The present study demonstrates that uterine cervical distension results in a similar pattern of spinal cord neuronal activation as seen with other noxious visceral stimuli. The inhibition of cFos expression by intrathecal ketorolac suggests that spinal cyclo-oxygenase plays a role in uterine cervical distension-induced nociception.

scholarly journals Ameliorative effect of apelin-13 against renal complications in L-NAME-induced preeclampsia in rats

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11110
Author(s):  
Reham Z. Hamza ◽  
Abdel Aziz A. Diab ◽  
Mansour H. Zahra ◽  
Ali K. Asalah ◽  
Mai S. Attia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Histopathological Examination ◽  
Female Rats ◽  
Serum Urea ◽  
Pregnant Rats ◽  
Arterial Blood ◽  
Total Urine

Pre-eclampsia (PE) accompanying acute liver and kidney injury has remained a master cause of both fetal and maternal mortality and morbidity. Vasoactive mediators, oxidative stress and inflammatory imbalanceshave an important role in PE pathogenesis. Apelin is an adipokine that improves endothelial dysfunction; has anti-inflammatory and antioxidant effects; moreover, its level reduced during PE. This study aimed to explore the effects of apelin-13 administration on preeclampsia-associated renal dysfunction and proteinuria. Thirty-three pregnant female rats were divided into three groups; group: 1 (normal pregnant rats), group: 2 (preeclamptic rats); where rats were injected subcutaneously with 75 mg L-NAME/ kg body weight/day beginning from 9th to 20th day of pregnancy andgroup 3 (apelin-13 treated preeclamptic rats); In which L-NAME-induced preeclamptic rats were subcutaneously injected with 6 × 10−8 mol apelin-13/kg body weight/twice daily starting from 6th to 20th day of pregnancy. In all groups, mean arterial blood pressure, total urine protein, serum urea, creatinine, nitric oxide (NO), endothelin-1 (ET-1), interleukin–6 (IL-6) and malondialdhyde (MDA) were measured. Histopathological examination of kidney tissues was also done. preeclamptic rats showed significantly increased mean arterial blood pressure, total urine proteins, serum urea, creatinine, ET-1, IL-6, and MDA, but revealed a significantly decreased serum NO level. On the other hand, apelin treatment significantly improved these parameters together with amelioration of kidney histoarchitecture in the treated group. In conclusion, apelin may be a potentially curative candidate for prohibiting kidney damage and have a therapeutic benefit in PE rat models.

Renal 20-HETE inhibition attenuates changes in renal hemodynamics induced by l-NAME treatment in pregnant rats

2005 ◽  
Vol 289 (5) ◽  
pp. F1116-F1122 ◽  
Author(s):  
Hui Huang ◽  
Yiqiang Zhou ◽  
Venugopal T. Raju ◽  
Juan Du ◽  
Hsin-Hsin Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Combined Treatment ◽  
Renal Hemodynamics ◽  
Female Rats ◽  
Control Group ◽  
Pregnant Rats ◽  
Functional Changes ◽  
No Inhibition ◽  
Renal Vascular

We previously reported that inhibition of nitric oxide (NO) synthesis by N-nitro-l-arginine methyl ester (l-NAME) during late pregnancy leads to increased production of renal vascular 20-hydroxyeicosatetraenoic acid (20-HETE), a cytochrome P-450 (CYP) 4A-derived vasoconstrictor, in pregnant rats. However, the effect of upregulation of vascular 20-HETE production on renal function after NO inhibition is not known. To test the hypothesis that increased gestational vascular 20-HETE synthesis after NO inhibition is involved in mediating blood pressure and renal functional changes, we first determined the IC50 value of the effect of nitroprusside (SNP), a NO donor, on renal 20-HETE production in cortical microsomes. We then divided pregnant rats and age-matched virgin rats into a vehicle control group, an l-NAME treatment group (0.25 mg/ml in drinking water), and a group treated with l-NAME plus N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS; CYP4A-selective inhibitor, 10 mg·kg−1·day−1 iv). After 4 days of treatment, we measured blood pressure, renal blood flow (RBF), renal vascular resistance (RVR), and glomerular filtration rate (GFR) in each group. The addition of SNP (IC50 = 22 μM) decreased renal cortical 20-HETE production. In pregnant rats, l-NAME treatment led to significantly higher mean arterial pressure (MAP) and RVR, and lower RBF and GFR. Combined treatment with DDMS and l-NAME significantly attenuated the increases in MAP and RVR and the decrease in GFR, but not the reduction in RBF induced by l-NAME treatment. l-NAME and l-NAME plus DDMS had no significant impact on renal hemodynamics in virgin rats. In addition, chronic treatment with DDMS selectively inhibited cortical 20-HETE production without a significant effect on CYP4A expression in l-NAME-treated pregnant rats. In conclusion, NO effectively inhibits renal cortical microsomal 20-HETE production in female rats. In pregnant rats, the augmentation of renal 20-HETE production after NO inhibition is associated with increased MAP and RVR, whereas decreased GFR is negated by treatment of a selective and competitive CYP4A inhibitor. These results demonstrate that the interaction between renal 20-HETE and NO is important in the regulation of renal function and blood pressure in pregnant rats.

scholarly journals Glomerular hemodynamic effects of late pregnancy in rats with experimental membranous glomerulonephropathy.

1995 ◽  
Vol 6 (4) ◽  
pp. 1197-1201
Author(s):  
C Baylis ◽  
A Deng ◽  
W G Couser
Keyword(s):  
Blood Pressure ◽  
Late Pregnancy ◽  
Systemic Blood Pressure ◽  
Female Rats ◽  
Pregnant Rats ◽  
Renal Vasoconstriction ◽  
Heymann Nephritis ◽  
Single Nephron ◽  
Glomerular Capillary Hypertension ◽  
Membranous Glomerulonephropathy

In these studies, the Fx1A model of accelerated, passive Heymann nephritis was used to produce membranous glomerulonephropathy. Female rats were studied at 7 wk after the administration of the Fx1A antibody either in the virgin state or in late pregnancy. The goals of these experiments were to determine whether preexisting membranous glomerulonephropathy compromises the pregnancy and whether the pregnancy acutely worsens the renal function. Virgin rats with membranous glomerulonephropathy developed massive proteinuria and exhibited glomerular capillary hypertension but without declines in GFR. In late pregnancy, there was no worsening of the proteinuria and glomerular blood pressure fell to normal values. Both afferent and efferent arteriolar resistances increased in pregnant rats with membranous glomerulonephropathy compared with virgins, leading to falls in glomerular plasma flow and single-nephron GFR. There were no histologic abnormalities in the glomeruli of either virgin or late pregnant rats with membranous glomerulonephropathy, and both groups exhibited similar immunoglobulin G and complement deposits. Up to Day 19 (term is 22 days), the pregnancy in rats with membranous glomerulonephropathy appeared uneventful. Thus, this study indicates that the Fx1A model of membranous glomerulonephropathy does not compromise the course of the pregnancy, at least until close to term. Pregnancy lowers glomerular blood pressure in rats with membranous glomerulonephropathy because of both a fall in systemic blood pressure and the atypical renal vasoconstriction, which leads to declines in single-nephron GFR.

scholarly journals Teratogenic Effect of Chlorpyrifos and Glyphosate on Pregnant Rats: Biochemical and Morphological Evaluations

2020 ◽  
pp. 133-145
Author(s):  
Jyoti Upadhyay ◽  
Mahendra Rana ◽  
Nidhi Tiwari ◽  
Mohd Nazam Ansari
Keyword(s):  
Spinal Cord ◽  
Exposed Group ◽  
Teratogenic Effect ◽  
The Body ◽  
Female Rats ◽  
Lactation Period ◽  
Pregnant Rats ◽  
Morphological Abnormalities ◽  
Rat Pups ◽  
The Impact

The impact of pesticides on the environment and human health is a serious matter of concern. The present study focusses on the teratogenic effect of pesticide chlorpyrifos (CPF) and glyphosate (GLY) on the pregnant rats and their offspring during gestation and lactation period. The female rats were exposed to these pesticides (CPF and GLY) throughout their pregnancy at a dose of 10 mg/kg. The biochemical markers and lipid profile of pesticides exposed pregnant rats were analyzed. The maternal and reproductive outcome was also assessed followed by rat pups morphometric analysis. A significant alteration in the blood glucose level, triglycerides, total cholesterol, SGOT, and SGPT levels were observed in pesticide exposed groups. The body weight, crown-rump length, eye length, eye width, hind limb, and forelimb size of rat neonates were significantly found to be lower in the pesticide exposed group when compared with the control animals. Morphological abnormalities like microcephaly, microtia, micromelia, dysmorphogenesis, distorted axis abdominal, and brain hemorrhages were observed in pesticide exposed rat neonates. Skeletal observations of the CPF exposed group show disruptive malformations, wavy ribs, and curved spinal cord. Intraventricular and spinal cord hemorrhages were observed in 21 days old rat pups in GLY treated group. Findings of the present study indicate that exposure to pesticides during the gestation period causes the morphological abnormalities in rat fetuses by altering the mechanisms involved in growth and development. Thus, on the basis of observed results, we concluded the teratogenic effects of CPF and GLY in rats.

Sign in / Sign up

Export Citation Format

Share Document