scholarly journals TOXICITY EVALUATION OF AMMONIUM SULFATE TO ALBINO RAT

Author(s):  
Siva Kumar T ◽  
Shobha Rani A ◽  
Sujatha K ◽  
Purushotham B ◽  
Neeraja P

ABSTRACTObjective: The present study was designed to find out the acute median lethal dose (LD50) of ammonium sulfate (inorganic fertilizer) in Wister albino rats.Methods: A single dose of ammonium sulfate dissolved in distilled water (Milli-Q) and administered intraperitoneally at concentrations of 10, 30, 50,70, 90, 110, 130, and 170 mg/kg body weight, respectively, to experimental animals, and then, they were observed every 3 hrs from prior dose giventime, later 6 hrs, 12 hrs, 24 hrs, to 48 hrs of noticing any abnormal behaviors and toxic signs, symptoms. After 48 hrs, counted the number of ratsdeparted in each group and mortality percentage was calculated.Results: The obtained results were evaluated by the Statistical Probit Analysis Method and 48 hrs LD value for albino rats was found tobe 91.5 mg/kg. At a single dose of 10 mg/kg, there is no morality and toxic behaviors were observed. Therefore, this concentration is considered asno observed adverse effect level dose.Conclusion: From the earlier consequences, identification and evaluation of the LD5050 against ammonium sulfate is crucial for understanding thehyperammonemia because ammonium sulfate has been highly utilized as inorganic fertilizer in agriculture and household gardens. Thus, theknowledge about toxic impacts of ammonia useful for clinical or toxicological approaches; however, the toxicity data are unclear. Hence, the in vitroLD50 evaluations of target chemical in Wistar rats is highly associated toward in ammonia-related peculiar disorders perceptive and therapy.Keywords: Ammonium sulfate, Fertilizer, Median lethal dose, Mortality, No observed adverse effect level.

2010 ◽  
Vol 29 (8) ◽  
pp. 645-652 ◽  
Author(s):  
YX Zou ◽  
XD Zhang ◽  
Y. Mao ◽  
GC Lu ◽  
M. Huang ◽  
...  

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to possess activity of inducing apoptosis in variety of tumor cells in preclinical models. Several mutational versions of TRAIL have been studied as promising agents for cancer therapy and the recombinant soluble human TRAIL mutant (DATR) is one of them. The objective of the present study was to provide possible toxic target organs and proposal non-toxic dose level of DATR for clinical usage. Rodents and crab-eating macaques were used to estimate potential adverse effects of DATR following a single dose administration. The median lethal dose (LD50 ) of intravenous injection to rats and mice was determined as 262.0 and 1018.0 mg/kg b.w., respectively. The LD50 of intraperitoneal administration to mice was found to be 1432.1 mg/kg b.w. The main changes in macaques were found in the following aspects. Hematology analysis revealed an obvious decrease of red blood cell count (RBC), hemoglobin (HB) and hematocrit (HCT) after injection. Serum biochemical analysis showed an apparent increase of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), blood urea nitrogen (BUN) and creatinine (Crea). Furthermore, inflammatory cell infiltrate in liver and kidney was found by microscope. All the disorders suggested that liver, renal and hematological systems might be the target effectors of toxic effect induced by DATR. Based on the results of this study, the no observed-adverse-effect level (NOAEL) and the lowest observed-adverse-effect level of DATR in macaques are 90.0 and 135.0 mg/kg b.w., respectively.


Toxicon ◽  
2020 ◽  
Vol 177 ◽  
pp. 16-24 ◽  
Author(s):  
Andrea Boente-Juncal ◽  
Carmen Vale ◽  
Mercedes Camiña ◽  
J. Manuel Cifuentes ◽  
Mercedes R. Vieytes ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Maitham Ahmed Al-Sammak ◽  
Douglas G. Rogers ◽  
Kyle D. Hoagland

The cyanobacterial neurotoxinβ-N-methylamino-L-alanine (BMAA) is considered to be an “excitotoxin,” and its suggested mechanism of action is killing neurons. Long-term exposure to L-BMAA is believed to lead to neurodegenerative diseases including Parkinson’s and Alzheimer’s diseases and amyotrophic lateral sclerosis (Lou Gehrig’s disease). Objectives of this study were to determine the presumptive median lethal dose (LD50), the Lowest-Observed-Adverse-Effect Level (LOAEL), and histopathologic lesions caused by the naturally occurring BMAA isomer, L-BMAA, in mice. Seventy NIH Swiss Outbred mice (35 male and 35 female) were used. Treatment group mice were injected intraperitoneally with 0.03, 0.3, 1, 2, and 3 mg/g body weight L-BMAA, respectively, and control mice were sham-injected. The presumptive LD50of L-BMAA was 3 mg/g BW and the LOAEL was 2 mg/g BW. There were no histopathologic lesions in brain, liver, heart, kidney, lung, or spleen in any of the mice during the 14-day study. L-BMAA was detected in brains and livers in all of treated mice but not in control mice. Males injected with 0.03 mg/g BW, 0.3 mg/g BW, and 3.0 mg/g BW L-BMAA showed consistently higher concentrations (P< 0.01) in brain and liver samples as compared to females in those respective groups.


2012 ◽  
Vol 31 (5) ◽  
pp. 441-453 ◽  
Author(s):  
Larry R. Williams ◽  
Valerie H. Adams ◽  
Shannon M. Wallace ◽  
Mark S. Johnson

Sustainable use of military training ranges requires the development of compounds that have a minimal impact to the environment when used in a weapon system. Guanidinium 3,4-dinitropyrazolate (GDNP) is a novel explosive compound of interest for application in some weapon systems. Little is known of its toxicologic properties. To ensure the health of potentially exposed personnel and the environment, initial toxicity investigations were conducted and the results were compared with another widely used energetic (hexahydro-1,3,5-trinitro-1,3,5-triazine [RDX]). In a microplate Ames assay, GDNP was not cytotoxic to bacterial tester strains at concentrations less than 100 μg/mL. However, GDNP was mutagenic to 4 of 5 bacterial strains with and without S9 metabolic incubation at concentrations as low as 0.7 μg/mL. Unlike RDX, GDNP did not have an affinity for the γ-aminobutyric acid(A) receptor convulsant site and was predicted to not induce seizure. After acute oral dosing in female rats, the median lethal dose in female rats of GDNP in tap water solution was determined to be 720 mg/kg. Daily oral exposure to 500 mg/kg per d of GDNP for 14 days caused weight loss, increased liver and spleen weights, and adverse histopathologic events in kidney and spleen. These adverse events were not observed in animals receiving lower doses of GDNP. In this study, the lowest-observed-adverse-effect-level from oral exposure to GDNP for 14 days was 500 mg/kg per d and the no-observable-adverse-effect-level was 152 mg/kg per d.


Toxins ◽  
2017 ◽  
Vol 9 (3) ◽  
pp. 75 ◽  
Author(s):  
Paula Abal ◽  
M. Louzao ◽  
Alvaro Antelo ◽  
Mercedes Alvarez ◽  
Eva Cagide ◽  
...  

2019 ◽  
Author(s):  
Simon Colas ◽  
Charlotte Duval ◽  
Benjamin Marie

AbstractThe proliferations of cyanobacteria are increasingly prevalent in warm and nutrient-enriched waters and occur in many rivers and water bodies due especially to eutrophication. The aim of this work is to study in female medaka fish the toxicity, the transfer and the depuration of the anatoxin-a, a neurotoxin produced by benthic cyanobacterial biofilms. This work will provide answers regarding acute toxicity induced by single gavage by anatoxin-a and to the risks of exposure by ingestion of contaminated fish flesh, considering that data on these aspects remain particularly limited.The oral LD50 of a single dose of (±)-anatoxin-a was determined at 11.50 µg.g−1. First of all, lethal dose (100% from 20 µg.g−1) provokes rapid respiratory paralysis (in 1-2 min) of the fish inducing the death by asphyxia. Noticeably, no death nor apparent neurotoxicologic effect occurred during the experimentation period for the 45 fish exposed to a single sub-acute dose of (±)-anatoxin-a corresponding to the no observable adverse effect level (NOAEL = 6.67 µg.g−1). Subsequently, the toxico-kinetics of the (±)-anatoxin-a was observed in the guts, the livers and the muscles of female medaka fish for 10 days.In parallel, a protocol for extraction of anatoxin-a has been optimized beforehand by testing 3 different solvents on several matrices, the extraction with 75% methanol + 0.1% formic acid appearing to be the most efficient. Anatoxin-a was quantified by high-resolution qTOF mass spectrometry coupled upstream to a UHPLC chromatographic chain. The toxin could not be detected in the liver after 12 h, and in the gut and muscle after 3 days. The mean clearance rates of (±)-anatoxin-a calculated after 12 h are above 58%, 100% and 90% for the guts, the livers and the muscles, respectively. Non-targeted metabolomics investigations performed on the fish liver indicates that the single sub-acute exposure by gavage induces noticeable metabolome dysregulations, including important phospholipid decreases, with an organism recovery period of above 12-24h. Overall, the medaka fish do not appear to accumulate (±)-anatoxin-a and to largely recover after 24h following a single sub-acute oral liquid exposure at the NOAEL.


1998 ◽  
Vol 14 (1-2) ◽  
pp. 311-323 ◽  
Author(s):  
Antonio Mutti ◽  
Audrey Smargiassi

Increased serum prolactin (PRL) is a common finding among subjects exposed to styrene, perchloroethylene, lead (Pb), and manganese (Mn) at levels below the current threshold limit values. On a group basis, abnormally high basal PRL shows a dose-related distribution among workers exposed to styrene, Pb, and Mn. On the basis of dose-response relationships, the benchmark doses (BMD) for styrene metabolites in urine, lead in blood (Pb-B), and Mn in urine (Mn-U), are 4 mg/g creatinine, 112 μg/L, and 0.3 μg/L, respectively. Noteworthy, the BMD for Mn-U and Pb-B is well below the upper reference limit. A shift in the distribution but not in the prevalence of abnormally high values of serum PRL was observed among perchloroethylene-exposed dry cleaners, which makes interpretation in terms of risk difficult. The measurement of PRL thus provides opportunities for early identification of excess exposure to neurotoxic chemicals affecting dopaminergic control of pituitary secretion. For styrene, Pb, and Mn the BMD provides an objective and statistically determined threshold, which seems to be in good agreement with the estimated no-observed-adverse-effect-level (NOAEL). The NOAEL, however, is based on traditional approaches that require the application of uncertainty factors, e.g., a default factor of 10 when extrapolating the NOAEL from the lowest-observed- adverse-effect-level (LOAEL). Due to its sensitivity to a number of potential confounders, caution must be exercised when using PRL as a screening test at the individual level. Also, age and sex dependent variations in susceptibility may hamper extrapolations from the occupational settings to the general population.


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