scholarly journals Inhalation toxicology of diesel-fuel obscurant aerosol in Sprague-Dawley rats. Chemical characterization and toxicological evaluation of airborne mixtures. Final report, phase 1, acute exposure

1983 ◽  
Author(s):  
W. Dalbey ◽  
S. Lock
2021 ◽  
pp. 112084
Author(s):  
Brianna J. Stubbs ◽  
Andrey I. Nikiforov ◽  
Marisa O. Rihner ◽  
Sari L. Weston ◽  
Nancy Higley ◽  
...  

2016 ◽  
Vol 90 ◽  
pp. 18-29 ◽  
Author(s):  
P. Mellado-García ◽  
M. Puerto ◽  
S. Pichardo ◽  
M. Llana-Ruiz-Cabello ◽  
R. Moyano ◽  
...  

2018 ◽  
Vol 88 (3-4) ◽  
pp. 199-208
Author(s):  
Elham Nikbakht ◽  
Rosita Jamaluddin ◽  
S. Mohd Redzwan ◽  
Saman Khalesi

Abstract. Aflatoxin B1 (AFB1) is a toxic compound commonly found in some crops with an adverse health effect on human and animals. Some beneficial microorganisms (or probiotics) such as lactic acid bacteria have shown the ability to reduce the bioavailability of aflatoxins and its intestinal absorption. However, the dose and duration of aflatoxins exposure and probiotic treatment can influence the ability of probiotics to remove aflatoxins. Therefore, this research aimed to investigate the efficacy of oral probiotic Lactobacillus casei Shirota strain (LcS) induction in an acute exposure to AFB1 in rats. Experimentally, Sprague Dawley rats were divided into three groups: AFB1 only (n = 9); AFB1 treated with LcS (n = 9); and control (no AFB1 exposure) (n = 6) groups. The blood AFB1 level of rats treated with LcS was slightly lower than the untreated AFB1 induced rats (11.12 ± 0.71 vs 10.93 ± 0.69 ng g–1). Also, LcS treatment slightly moderated the liver and kidney biomarkers in AFB1 induced rats. However, a trend for a significant difference was only observed in ALT of AFB1 induced rats treated with LcS compared to their counterparts (126.11 ± 36.90 vs 157.36 ± 15.46, p = 0.06). Rats’ body weight decreased in all animals force-fed with AFB1 with no significant difference between LcS treatment compared to the counterpart. In conclusion, this experiment indicated that probiotic LsC was able to slightly ameliorate the adverse effect of an acute exposure to AFB1 in rats. However, future studies with longer probiotics treatment or higher probiotics dose is required to confirm these findings.


2005 ◽  
Vol 22 (3) ◽  
pp. 259-269 ◽  
Author(s):  
Evans Afriyie-Gyawu ◽  
John Mackie ◽  
Bhagirathi Dash ◽  
Melinda Wiles ◽  
John Taylor ◽  
...  

2001 ◽  
Vol 281 (4) ◽  
pp. E867-E877 ◽  
Author(s):  
R. Tupling ◽  
H. Green ◽  
G. Senisterra ◽  
J. Lepock ◽  
N. McKee

To investigate the hypothesis that ischemia and reperfusion would impair sarcoplasmic reticulum (SR) Ca2+ regulation in skeletal muscle, Sprague-Dawley rats ( n = 20) weighing 290 ± 3.5 g were randomly assigned to either a control control (CC) group, in which only the effects of anesthetization were studied, or to a group in which the muscles in one hindlimb were made ischemic for 4 h and allowed to recover for 1 h (I). The nonischemic, contralateral muscles served as control (C). Measurements of Ca2+-ATPase properties in homogenates and SR vesicles, in mixed gastrocnemius and tibialis anterior muscles, indicated no differences between groups on maximal activity, the Hill coefficient, and Ca50, defined as the Ca2+concentration needed to elicit 50% of maximal activity. In homogenates, Ca2+ uptake was lower ( P < 0.05) by 20–25%, measured at 0.5 and 1.0 μM of free Ca2+ ([Ca2+]f) in C compared with CC. In SR vesicles, Ca2+ uptake was lower ( P < 0.05) by 30–38% in I compared with CC at [Ca2+]f between 0.5 and 1.5 μM. Silver nitrate induced Ca2+ release, assessed during both the initial, early rapid ( phase 1), and slower, prolonged late ( phase 2) phases, in homogenates and SR vesicles, indicated a higher ( P < 0.05) release only in phase 1in SR vesicles in I compared with CC. These results indicate that the alterations in SR Ca2+ regulation, previously observed after prolonged ischemia by our group, are reversed within 1 h of reperfusion. However, the lower Ca2+ uptake observed in long-term, nonischemic homogenates suggests that altered regulation may occur in the absence of ischemia.


2001 ◽  
Vol 281 (2) ◽  
pp. E224-E232 ◽  
Author(s):  
R. Tupling ◽  
H. Green ◽  
G. Senisterra ◽  
J. Lepock ◽  
N. McKee

In this study, we investigated the hypothesis that prolonged ischemia would impair both sarcoplasmic reticulum (SR) Ca2+ uptake and Ca2+ release in skeletal muscle. To induce total ischemia (I), a tourniquet was placed around the upper hindlimb in 30 female Sprague-Dawley rats [wt = 256 ± 6.7 (SE) g] and inflated to 350 mmHg for 4 h. The contralateral limb served as control (C). Immediately after the 4 h of ischemia, mixed gastrocnemius and tibialis anterior muscle was sampled from both limbs, and both crude muscle homogenates and SR vesicles were prepared. In another 10 control animals (CC), muscles were sampled and prepared exactly the same way, but immediately after anesthetization. Ca2+ uptake and Ca2+ release were measured in vitro with Indo-I on both homogenates and SR vesicles. As hypothesized, submaximal Ca2+ uptake was lower ( P < 0.05) in I compared with CC and C, by 25 and 45% in homogenates and SR vesicles, respectively. Silver nitrate (AgNO3)-induced Ca2+ release, which occurred in two phases ( phase 1 and phase 2), was also altered in I compared with CC and C, in both muscle homogenates and SR vesicles. With ischemia, phase 1 peak Ca2+ release was 26% lower ( P < 0.05) in SR vesicles only. For phase 2, peak Ca2+ release was 54 and 24% lower ( P < 0.05) in SR vesicles and homogenates, respectively. These results demonstrate that prolonged skeletal muscle ischemia leads to a reduced SR Ca2+uptake in both homogenates and SR vesicles. The effects of ischemia on SR Ca2+ release, however, depend on both the phase examined and the type of tissue preparation.


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