The Effects of Jp-8 Jet Fuel on Male Sprague-Dawley Rats after a 90-Day Exposure By Oral Gavage

1995 ◽  
Vol 11 (4) ◽  
pp. 423-435 ◽  
Author(s):  
David R. Mattie ◽  
Gary B. Marit ◽  
Carlyle D. Flemming ◽  
James R. Cooper
Keyword(s):  
Adverse Effects ◽  
Jet Fuel ◽  
Additional Treatment ◽  
Male Rats ◽  
Male Rat ◽  
Oral Exposure ◽  
Sprague Dawley ◽  
Weight Changes ◽  
Inhalation Study ◽  
Dose Dependent

The U.S. Air Force is converting from JP-4 jet fuel to the less volatile JP-8 jet fuel, which is similar to commercial Jet Fuel A. Our previous 90-day inhalation study with JP-8 vapor, using F-344 rats and C57BL/6 mice, resulted in no treatment-related adverse effects other than α 2-microglobin nephropathy in male rats (Mattie et al., 1991). In the present study, male rats were dosed with neat JP-8 (0, 750, 1500, 3000 mg/kg) daily by gavage for 90 days in an effort to characterize the kidney lesion and assess further any additional adverse effects associated with prolonged oral exposure to this fuel. Results of this study revealed a significant dose-dependent decrease in body weights of rats exposed to JP-8. Male rat-specific α 2-microglobin nephropathy was observed by histopathologic examination. A number of significant changes were also seen in blood and urine that were not dose-dependent. Additional treatment-related effects were a gastritis and a perianal dermatitis. Although there were no histopathological or weight changes in the livers of exposed rats, there was an increase in the liver enzymes AST and ALT. The elevated enzymes did not increase with increasing dose of JP-8.

Toxicity Evaluation of Petroleum Blending Streams: Inhalation Subchronic Toxicity/Neurotoxicity Study of a Light Catalytic Cracked Naphtha Distillate in Rats

2001 ◽  
Vol 20 (5) ◽  
pp. 307-319 ◽  
Author(s):  
C. Lapin ◽  
Q. Bui ◽  
R. Breglia ◽  
F. Koschier ◽  
P. Podhasky ◽  
...  
Keyword(s):  
Body Weight Gain ◽  
Clinical Chemistry ◽  
Male Rats ◽  
Whole Body ◽  
Male Rat ◽  
Exposure Level ◽  
Sprague Dawley ◽  
Subchronic Toxicity ◽  
High Exposure ◽  
Inhalation Study

A 15-week, whole-body inhalation study of the vapors of a distillate (LCCN-D) of light catalytic cracked naphtha (CAS no. 64741–55–5, LCCN) was conducted with Sprague-Dawley rats. Target exposure concentrations were 0, 750, 2500, and 7500 ppm for 6 hours/day, 5 days/week. Over the course of the study, animals received at least 65 exposures. For a portion of the control and 7500-ppm groups, a 4-week postexposure period was included in the study. Subchronic toxicity was evaluated using standard parameters. During life, neurotoxicity was evaluated by motor activity assessment and a functional observational battery. Selected tissues from animals in all exposure groups were examined microscopically. Neuropathologic examination of selected neuronal tissues from animals in the control and high-exposure groups was also conducted. No compound-related effects were seen on survival, clinical chemistry, food consumption, or physical signs. No evidence of neurotoxicity was seen at any exposure level. Slight decreases in hematocrit and hemoglobin concentrations were seen in male rats at the end of exposure to 7500 ppm LCCN-D. However, values were within normal physiological ranges and recovery occurred. Slight decreases in mean body weights and body weight gain were observed in high-exposure females during the first 7 weeks of exposure, but this decrease was not seen during the second half of the study. Male rat nephropathy involving hyaline droplet formation and alpha-2μ-globulin accumulation was seen in mid-and high-exposure males, an effect not relevant to humans. The incidence and severity of goblet cell hypertrophy/hyperplasia and respiratory epithelium hyperplasia in nasoturbinal tissues were greater in high-exposure animals, but recovery occurred. None of the effects observed were considered toxicologically significant. The no-observable-adverse-effect level (NOAEL) for subchronic and neurotoxicity of LCCN-D was ≥7500 ppm.

Refining the Effects Observed in a Developmental Neurobehavioral Study of Ammonium Perchlorate Administered Orally in Drinking Water to Rats. II. Behavioral and Neurodevelopment Effects

2005 ◽  
Vol 24 (6) ◽  
pp. 451-467 ◽  
Author(s):  
Raymond G. York ◽  
John Barnett ◽  
Michael F. Girard ◽  
David R. Mattie ◽  
Marni V. K. Bekkedal ◽  
...  
Keyword(s):  
Drinking Water ◽  
Ammonium Perchlorate ◽  
Brain Regions ◽  
Male Rats ◽  
Male Rat ◽  
Sprague Dawley ◽  
Continuous Access ◽  
Brain Morphometry ◽  
The Central Nervous System ◽  
The Right

A developmental neurotoxicity study was conducted to generate additional data on the potential functional and morphological hazard to the central nervous system caused by ammonium perchlorate in offspring from in utero and lactation exposure. Female Sprague-Dawley rats (23 to 25/group) were given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 10.0 mg/kg-day perchlorate in the drinking water beginning 2 weeks prior to mating and continuing through day 10 of lactation for the behavioral function assessment or given continuous access to 0 (carrier), 0.1, 1.0, 3.0, and 30.0 mg/kg-day beginning on gestation day 0 and continuing through day 10 of lactation for neurodevelopment assessments. Motor activity was conducted on postpartum days 14, 18, and 22 and juvenile brain weights, neurohistopathological examinations, and regional brain morphometry were conducted on postpartum days 10 and 22. This research revealed a sexually dimorphic response, with some brain regions being larger in perchlorate-treated male rats than in comparable controls. Even so, there was no evidence of any obvious exposure-related effects on male rat brain weights or neuropathology. The most consistent exposure-related effect in the male pups was on the thickness of the corpus callosum, with both the right- and left-sided measures of the thickness of this white matter tract being significantly greater for the male pups in the 0.1 and 1.0 mg/kg-day exposure groups. The behavioral testing suggests prenatal exposure to ammonium perchlorate does not affect the development of gross motor movements in the pups.

scholarly journals Final Report on the Safety Assessment of Stearoxy Dimethicone, Dimethicone, Methicone, Amino Bispropyl Dimethicone, Aminopropyl Dimethicone, Amodimethicone, Amodimethicone Hydroxystearate, Behenoxy Dimethicone, C24–28 Alkyl Methicone, C30–45 Alkyl Methicone, C30–45 Alkyl Dimethicone, Cetearyl Methicone, Cetyl Dimethicone, Dimethoxysilyl Ethylenediaminopropyl Dimethicone, Hexyl Methicone, Hydroxypropyldimethicone, Stearamidopropyl Dimethicone, Stearyl Dimethicone, Stearyl Methicone, and Vinyldimethicone

2003 ◽  
Vol 22 (2_suppl) ◽  
pp. 10-35
Keyword(s):  
Adverse Effects ◽  
Expert Panel ◽  
Developmental Toxicity ◽  
Oral Exposure ◽  
Final Report ◽  
Short Term ◽  
Fluid Mixture ◽  
Inhalation Study ◽  
Cosmetic Formulations ◽  
Siloxane Polymers

Dimethicone is a fluid mixture of fully methylated linear siloxane polymers end-blocked with trimethylsiloxy units. Methicone is a linear monomethyl polysiloxane. The other dimethicones and methicones covered in this review are siloxane polymers of Dimethicone and Methicone. Most of these ingredients function as conditioning agents in cosmetic formulations at current concentrations of use of ≤ 15%. Clinical and animal absorption studies reported that Dimethicone was not absorbed following oral or dermal exposure. Dimethicone, Methicone, and Vinyldimethicone were not acutely toxic following oral exposure. No adverse reactions were found in rabbits following short-term dermal dosing with 6% to 79% Dimethicone, yet adverse effects were noted with a hand cream formulation containing 1% Dimethicone, suggesting something else in the preparation was toxic. Mice and rats were dosed for 90 days with up to 10% Dimethicone without adverse effect. Dimethicone did not produce adverse effects in acute and short-term inhalation-route studies, Methicone and Vinyldimethicone were negative in acute exposure studies using rats, but Hexyl Methicone was toxic to rats at 5 mg/L delivered in small particle (mean diameter of 0.29 μ) aerosols. Most dermal irritation studies using rabbits classified Dimethicone as a minimal irritant. Dimethicone (tested undiluted and at 79%) was not a sensitizer in four assays using mice and guinea pigs. It was not a sensitizer at 5.0% in a clinical repeated insult patch test using 83 panelists. Most ocular irritation studies using rabbits classified Dimethicone as a mild to minimal irritant. Dimethicone was tested in numerous oral-dose (using rats) and dermal-dose (using rats, rabbits, and monkeys) reproductive and developmental toxicity studies. In a few studies, treated males had significantly decreased body weight and/or decreased testes or seminal vesicles weights. No treatment-related adverse findings were noted in dosed pregnant females or fetuses. Dimethicone was negative in all genotoxicity assays. It was negative in both an oral (tested at 91%) and dermal (tested at an unknown concentration) dose carcinogenicity assay using mice. The Cosmetic Ingredient Review (CIR) Expert Panel considered it unlikely that any of these polymers would be significantly absorbed into the skin due to their large molecular weight. Although adverse effects were noted in one inhalation study with small aerosol particles, the expected particle sizes for cosmetic products would primarily be in the range of 60 to 80 μ, and less than 1% would be under 10 μ, which is an upper limit for respirable particles. Overall, the safety test data support the safety of these ingredients at the concentrations they are known to be used in cosmetic formulations. Accordingly, the CIR Expert Panel was of the opinion that Stearoxy Dimethicone, Dimethicone, Methicone, Amino Bis-propyl Dimethicone, Aminopropyl Dimethicone, Amodimethicone, Amodimethicone Hydroxystearate, Behenoxy Dimethicone, C24–28 Alkyl Methicone, C30–45 Alkyl Methicone, C30–45 Alkyl Dimethicone, Cetearyl Methicone, Cetyl Dimethicone, Dimethoxysilyl Ethylenediaminopropyl Dimethicone, Hexyl Methicone, Hydroxypropyldimethicone, Stearamidopropyl Dimethicone, Stearyl Dimethicone, Stearyl Methicone, and Vinyldimethicone are safe as used in cosmetic formulations.

scholarly journals Dose-dependent acceleration in the delayed effects of neonatal oral exposure to low-dose 17α-ethynylestradiol on reproductive functions in female Sprague-Dawley rats

2015 ◽  
Vol 40 (6) ◽  
pp. 727-738 ◽  
Author(s):  
Mariko Shirota ◽  
Jun Kawashima ◽  
Tomohiro Nakamura ◽  
Junichi Kamiie ◽  
Kinji Shirota ◽  
...  
Keyword(s):  
Low Dose ◽  
Oral Exposure ◽  
Sprague Dawley ◽  
Delayed Effects ◽  
Sprague Dawley Rats ◽  
Dose Dependent

scholarly journals Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials

2014 ◽  
Vol 65 (4) ◽  
pp. 387-398 ◽  
Author(s):  
Mustafa Yardimci ◽  
Yusuf Sevgiler ◽  
Eyyup Rencuzogullari ◽  
Mehmet Arslan ◽  
Mehmet Buyukleyla ◽  
...  
Keyword(s):  
Cholinesterase Activity ◽  
Specific Effect ◽  
Piperonyl Butoxide ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Total Protein Content ◽  
Sprague Dawley ◽  
Adverse Action ◽  
Liver And Kidney

Abstract Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid’s adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg-1) or in combination with piperonyl butoxide (100 mg kg-1) or menadione (25 mg kg-1) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity

Subchronic Toxicity Study of Dicyclopentadiene Vapor in Rats

1992 ◽  
Vol 8 (6) ◽  
pp. 353-367 ◽  
Author(s):  
Christopher Bevan ◽  
William M. Snellings ◽  
Darol E. Dodd ◽  
Gerard F. Egan
Keyword(s):  
Epithelial Cells ◽  
Clinical Chemistry ◽  
Recovery Period ◽  
Proximal Tubules ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Weight Changes ◽  
High Exposure ◽  
Excretion Rates

Fischer 344 rats were exposed by inhalation to 0, 1, 5 or 50 ppm dicyclopentadiene (DCPD) vapor 6 hr/day, 5 days/week for 13 weeks, followed by a 13-week recovery period. Animals were euthanized following completion of exposure at 2, 6, or 13 weeks and at postexposure weeks 4 or 13. No mortality, overt signs, body weight changes, hematologic or clinical chemistry values were related to DCPD exposure. In the high-exposure male rats, relative liver weights were significantly increased but with no accompanying histopathologic changes. Exposure to DCPD produced adverse kidney effects in male, but not female, rats as evidenced by the excretion of epithelial cells in the urine. Histologic changes were localized to the proximal tubules of the kidney and included increased accumulation of protein droplets, regenerative epithelium, and the presence of intraluminal proteinaceous material. In addition, several alterations in renal function were observed. Urinary Na+ excretion rates were decreased and urinary K+ excretion rates were increased throughout the exposure period; however, glucose was not present in the urine, and creatinine clearance was normal. The ability of the kidney to concentrate urine was also impaired. After the recovery period, many of the treatment-related kidney effects were not observed, including the presence of hyaline droplets in the proximal tubules and epithelial cells in the urine. These findings indicate an overall low degree of systemic toxicity following sub-chronic inhalation exposure of dicyclopentadiene at exposure levels up to 50 ppm. The only effect that was observed was a male rat-specific nephropathy that is characteristic of the hyaline droplet nephropathy produced by a diverse group of compounds.

scholarly journals Effect of I-131 incorporation on male rat reproductive system and the dose-dependent effect

1994 ◽  
Vol 40 (3) ◽  
pp. 45-47
Author(s):  
L. V. Tarasenko ◽  
S. V. Varga ◽  
V. N. Demchenko ◽  
Ye. V. Bolshova ◽  
N. D. Nosenko ◽  
...  
Keyword(s):  
Reproductive System ◽  
Biologically Active ◽  
Male Rats ◽  
Male Rat ◽  
Dependent Effect ◽  
Functional Changes ◽  
System A ◽  
Direct Injury ◽  
Dose Dependent ◽  
Dose Dependent Effect

Radioactive 131Iwas injected in single doses 9.25, 37, and 92.5 kBq to prepubertal (30-day-old) male rats. Iodine incorporation in doses 37 and 92.5 kBq resulted in some functional changes in the reproductive system of mature rats: blood testosterone level increased, its hypothalamic aromatization intensified, and biologically active LH level in the blood dropped. Incorporation of 9.25 kBq of 131-I had no effect on male reproductive system. A possibility of direct injury to rat testicles by 131I incorporation is suggested.

scholarly journals Intergenerational Effects of Sevoflurane in Young Adult Rats

2019 ◽  
Vol 131 (5) ◽  
pp. 1092-1109 ◽  
Author(s):  
Ling-Sha Ju ◽  
Jiao-Jiao Yang ◽  
Ning Xu ◽  
Jia Li ◽  
Timothy E. Morey ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Prepulse Inhibition ◽  
Germ Cells ◽  
Elevated Plus Maze ◽  
Acoustic Startle ◽  
Chloride Ion ◽  
Male Rats ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Plus Maze

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Sevoflurane administered to neonatal rats induces neurobehavioral abnormalities and epigenetic reprogramming of their germ cells; the latter can pass adverse effects of sevoflurane to future offspring. As germ cells are susceptible to reprogramming by environmental factors across the lifespan, the authors hypothesized that sevoflurane administered to adult rats could induce neurobehavioral abnormalities in future offspring, but not in the exposed rats themselves. Methods Sprague-Dawley rats were anesthetized with 2.1% sevoflurane for 3 h every other day between postnatal days 56 and 60. Twenty-five days later, exposed rats and nonexposed controls were mated to produce offspring. Results Adult male but not female offspring of exposed parents of either sex exhibited deficiencies in elevated plus maze (mean ± SD, offspring of both exposed parents vs. offspring of control parents, 35 ± 12 vs. 15 ± 15 s, P < 0.001) and prepulse inhibition of acoustic startle (offspring of both exposed parents vs. offspring of control parents, 46.504 ± 13.448 vs. 25.838 ± 22.866%, P = 0.009), and increased methylation and reduced expression of the potassium ion-chloride ion cotransporter KCC2 gene (Kcc2) in the hypothalamus. Kcc2 was also hypermethylated in sperm and ovary of the exposed rats. Surprisingly, exposed male rats also exhibited long-term abnormalities in functioning of the hypothalamic-pituitary-gonadal and -adrenal axes, reduced expression of hypothalamic and hippocampal Kcc2, and deficiencies in elevated plus maze (sevoflurane vs. control, 40 ± 24 vs. 25 ± 12 s, P = 0.038) and prepulse inhibition of startle (sevoflurane vs. control, 39.905 ± 21.507 vs. 29.193 ± 24.263%, P < 0.050). Conclusions Adult sevoflurane exposure affects brain development in male offspring by epigenetically reprogramming both parental germ cells, while it induces neuroendocrine and behavioral abnormalities only in exposed males. Sex steroids may be required for mediation of the adverse effects of adult sevoflurane in exposed males.

Reproductive toxicity of DDT in adult male rats

2001 ◽  
Vol 20 (8) ◽  
pp. 393-397 ◽  
Author(s):  
K Ben Rhouma ◽  
O Tébourbi ◽  
R Krichah ◽  
M Sakly
Keyword(s):  
Adult Male ◽  
Pesticide Exposure ◽  
Reproductive Toxicity ◽  
Male Rats ◽  
Male Rat ◽  
Seminiferous Tubules ◽  
Serum Lh ◽  
Testicular Weight ◽  
Hypothalamic Pituitary Axis ◽  
Dose Dependent

The reproductive toxicity of DDT was investigated in adult male rats exposed to 50 and 100 mg/kg body weight (b.wt) day 1 for 10 successive days. Compared with control animals, administration of DDT led to a dose-dependent reduction of testicular weight and the number as well as the percentage of motile spermatozoa in the epididymis. Testicular histological observationsrevealed alsoamarkedloss of gametes in the lumen of seminiferous tubules. In DDT treated rats, the seminal vesicles weights dropped significantly, resulting from a decrease of testosterone production by testes, whereas serum LH and FSH increased after pesticide exposure. This increase of gonadotrophin levels may be related to an impairment of the negative feedback exerted by the steroid on the hypothalamic–pituitary axis. It is concluded that DDT induced adverse effects on male rat fertility by acting directly on the testes and altering the neuroendocrinefunction.

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