scholarly journals Effect of garlic extract on mortality and biochemical parameters of fresh water fishes Heteropneustes fossilis against Cypermethrin

2019 ◽  
Vol 9 (2) ◽  
pp. 14-19
Author(s):  
Akanksha Singh ◽  
Kaneez Zahra

To find out the effect of garlic extract (GE) on mortality different concentrations of GE (1ml/l, 2ml/l, 5ml/l & 10ml/l) were administered along with the LC50 values of cypermethrin after 24, 48, 72 & 96 h exposures and 10 ml/l of GE was found to be effective at which no mortality occurred. To analyze the effect of GE on biochemical parameters after acute exposure of cypermethrin, fishes were divided into 4 groups of 10 fishes each. Ist group served as control, IInd, IIIrd and IVth group were treated with toxicant (24h LC50), GE (10ml/l) and toxicant + GE respectively. Same protocol was employed using 48-96 h LC50 values & 10ml/l GE. For chronic toxicity experiments fishes were divided into 4 groups of 10 fishes each. Ist group taken as control, IInd group contained 1/10th of 96 h LC50 of CYP, IIIrd group contained 10ml/l GE and in IVth group GE (10ml/l) + CYP (1/10th of 96 h LC50) for 15 days. Experiments were also carried out after 30 and 45 days exposure by same protocol. After acute and chronic exposure periods blood samples were collected, centrifuged and serum was separated to analyze biochemical parameters. Increased level of SGOT, SGPT, ALP, ACP, Creatinine, and Blood Glucose were observed during both acute and chronic exposure. Activity of Total protein was found to be decreased following acute and chronic exposure. Level of Uric acid increased in acute exposure but decreased during chronic exposure. However, garlic extract supplementation showed a remarkable reduction to these changes and all the parameters tends to become normalize. Our data indicate that garlic is a powerful antioxidant against cypermethrin induced toxicity. Keywords: Cypermethrin, Garlic extract, Heteropneustus fossilis, LC50.

2021 ◽  
Vol 12 (6) ◽  
pp. 35-39
Author(s):  
Adeeba Anjum ◽  
Ashik Mosaddik ◽  
Mir Imam Ibne Wahed ◽  
Md. Ekramul Haque

The current study was carried out to investigate the sub-acute toxicity of 3-O--D-glucopyranosyl-(24)-ethylcholesta-5,22,25-triene, a steroidal glycoside isolated from the flowers of Alangium salviifolium Wang on Long Evan’s rat. After intra-peritoneal administration of the compound at a dose of 300 μg/rat/day for 14 consecutive days, no mortality or significant changes in body weight or behavior were observed. The blood samples of the rats were examined for hematological and biochemical parameters which were statistically insignificant when compared to that of the control group. All the vital organs showed normal histopathological architecture (heart, lungs, liver and kidney) in comparison to the control group. This preliminary investigation demonstrate that the compound is safe at dose of 300 μg/rat/day for 14 consecutive days. But acute, sub-chronic and chronic toxicity evaluations as well as clinical trials need to be done.


2002 ◽  
Vol 30 (2_suppl) ◽  
pp. 101-105 ◽  
Author(s):  
Pilar Prieto

In many organs of the human body, there are effective physiological barriers which contribute to regulation of the uptake, transport and secretion of endogenous and exogenous materials. ECVAM is involved in the development of several in vitro models for detecting damage to various barriers, including, the renal epithelium, the intestinal barrier, and the blood–brain barrier, after acute and chronic exposure to chemicals and products of various kinds. Long-term toxicity testing is an important issue in toxicology. At present, there are no generally accepted in vitro models available for replacing chronic testing in animals. Under chronic exposure conditions, the cellular response is greater than that which can be predicted in the standard cytotoxicity models. Therefore, the approach to predicting chronic toxicity will need to involve more-complex in vitro models. Several currently available in vitro long-term toxicity systems are under evaluation.


PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12486
Author(s):  
Edward A. Straw ◽  
Mark J.F. Brown

Background Glyphosate is the world’s most used pesticide and it is used without the mitigation measures that could reduce the exposure of pollinators to it. However, studies are starting to suggest negative impacts of this pesticide on bees, an essential group of pollinators. Accordingly, whether glyphosate, alone or alongside other stressors, is detrimental to bee health is a vital question. Bees are suffering declines across the globe, and pesticides, including glyphosate, have been suggested as being factors in these declines. Methods Here we test, across a range of experimental paradigms, whether glyphosate impacts a wild bumble bee species, Bombus terrestris. In addition, we build upon existing work with honey bees testing glyphosate-parasite interactions by conducting fully crossed experiments with glyphosate and a common bumble bee trypanosome gut parasite, Crithidia bombi. We utilised regulatory acute toxicity testing protocols, modified to allow for exposure to multiple stressors. These protocols are expanded upon to test for effects on long term survival (20 days). Microcolony testing, using unmated workers, was employed to measure the impacts of either stressor on a proxy of reproductive success. This microcolony testing was conducted with both acute and chronic exposure to cover a range of exposure scenarios. Results We found no effects of acute or chronic exposure to glyphosate, over a range of timespans post-exposure, on mortality or a range of sublethal metrics. We also found no interaction between glyphosate and Crithidia bombi in any metric, although there was conflicting evidence of increased parasite intensity after an acute exposure to glyphosate. In contrast to published literature, we found no direct impacts of this parasite on bee health. Our testing focussed on mortality and worker reproduction, so impacts of either or both of these stressors on other sublethal metrics could still exist. Conclusions Our results expand the current knowledge on glyphosate by testing a previously untested species, Bombus terrestris, using acute exposure, and by incorporating a parasite never before tested alongside glyphosate. In conclusion our results find that glyphosate, as an active ingredient, is unlikely to be harmful to bumble bees either alone, or alongside Crithidia bombi.


2019 ◽  
Vol 7 (9) ◽  
pp. 325
Author(s):  
Haihong Hao ◽  
Kuppan Gokulan ◽  
Silvia A. Piñeiro ◽  
Katherine M. Williams ◽  
Zonghui Yuan ◽  
...  

Residual concentrations of erythromycin in food could result in gastrointestinal tract exposure that potentially poses a health-hazard to the consumer, affecting intestinal epithelial permeability, barrier function, microbiota composition, and antimicrobial resistance. We investigated the effects of erythromycin after acute (48 h single treatment with 0.03 μg/mL to 300 μg/mL) or chronic (repeated treatment with 0.3 µg/mL and 300 µg/mL erythromycin for five days) exposures on the permeability of human colonic epithelial cells, a model that mimics a susceptible intestinal surface devoid of commensal microbiota. Transepithelial electrical resistance (TER) measurements indicated that erythromycin above 0.3 µg/mL may compromise the epithelial barrier. Acute exposure increased cytotoxicity, while chronic exposure decreased the cytotoxicity. Quantitative PCR analysis revealed that only ICAM1 (intercellular adhesion molecule 1) was up-regulated during 0.3 μg/mL acute-exposure, while ICAM1, JAM3 (junctional adhesion molecule 3), and ITGA8 (integrin alpha 8), were over-expressed in the 300 μg/mL acute treatment group. However, during chronic exposure, no change in the mRNA expression was observed at 0.3 μg/mL, and only ICAM2 was significantly up-regulated after 300 μg/mL. ICAM1 and ICAM2 are known to be involved in the formation of extracellular matrices. These gene expression changes may be related to the immunoregulatory activity of erythromycin, or a compensatory mechanism of the epithelial cells to overcome the distress caused by erythromycin due to increased permeability.


2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 143-143
Author(s):  
Lionel Lloyds Banez ◽  
Anthony Kyle Davidson ◽  
Wiguins Etienne ◽  
Emma H Allott ◽  
Elizabeth Ellen Calloway ◽  
...  

143 Background: We recently reported that the ADH1B*3 allele, which is specific to African Americans (AA), when combined with ethanol intake may constitute a gene-environment interaction leading to elevated prostate cancer (CaP) and potentially aggressive CaP risk among AA men possibly through intra-prostatic acetaldehyde accumulation. Indeed, studies have shown microsomes from rat ventral prostates biotransform ethanol to acetaldehyde that further metabolizes into oxidative stress-inducing acetyl radicals. In addition, acetaldehyde has been previously shown to enhance proliferation of colon cancer cells. Whether acetaldehyde has the same effect on CaP is unknown. Methods: We subjected DU-145 CaP cells to varying concentrations of acetaldehyde using acute and chronic models of exposure and measured tumor proliferation using MTS assay. Proliferation was measured over 4 days of acetaldehyde treatment in acute and after 2 weeks of treatment in chronic exposure experiments. All experiments were conducted in triplicate. Results were expressed as mean values for each treatment referenced to untreated cells. Doubling times were calculated using least squares fitting exponential regression. Results: In the acute exposure model, proliferation of DU-145 cells was inhibited by 150 uM acetaldehyde by 28% while 1,500uM and higher concentrations resulted in complete inhibition of proliferation. After chronic exposure to acetaldehyde, proliferation of DU-145 cells was inhibited by 500 uM acetaldehyde by 19%. In contrast, chronic exposure with 1,000 uM acetaldehyde resulted in increased proliferation by 9% and shortened tumor doubling time. Conclusions: Acute exposure to acetaldehyde resulted in inhibition of CaP cellular proliferation. Chronic exposure to high acetaldehyde concentrations promoted tumor proliferation likely through selection for more robust CaP cells that survive the repeated chemical insult. Our results suggest that chronic acetaldehyde exposure of existent CaP may potentially promote disease aggressiveness. Uncovering mechanisms for enhanced CaP cell proliferation by acetaldehyde are warranted.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Patrick D. M. C. Katoto ◽  
Amanda S. Brand ◽  
Buket Bakan ◽  
Paul Musa Obadia ◽  
Carsi Kuhangana ◽  
...  

Abstract Background Air pollution is one of the world’s leading mortality risk factors contributing to seven million deaths annually. COVID-19 pandemic has claimed about one million deaths in less than a year. However, it is unclear whether exposure to acute and chronic air pollution influences the COVID-19 epidemiologic curve. Methods We searched for relevant studies listed in six electronic databases between December 2019 and September 2020. We applied no language or publication status limits. Studies presented as original articles, studies that assessed risk, incidence, prevalence, or lethality of COVID-19 in relation with exposure to either short-term or long-term exposure to ambient air pollution were included. All patients regardless of age, sex and location diagnosed as having COVID-19 of any severity were taken into consideration. We synthesised results using harvest plots based on effect direction. Results Included studies were cross-sectional (n = 10), retrospective cohorts (n = 9), ecological (n = 6 of which two were time-series) and hypothesis (n = 1). Of these studies, 52 and 48% assessed the effect of short-term and long-term pollutant exposure, respectively and one evaluated both. Pollutants mostly studied were PM2.5 (64%), NO2 (50%), PM10 (43%) and O3 (29%) for acute effects and PM2.5 (85%), NO2 (39%) and O3 (23%) then PM10 (15%) for chronic effects. Most assessed COVID-19 outcomes were incidence and mortality rate. Acutely, pollutants independently associated with COVID-19 incidence and mortality were first PM2.5 then PM10, NO2 and O3 (only for incident cases). Chronically, similar relationships were found for PM2.5 and NO2. High overall risk of bias judgments (86 and 39% in short-term and long-term exposure studies, respectively) was predominantly due to a failure to adjust aggregated data for important confounders, and to a lesser extent because of a lack of comparative analysis. Conclusion The body of evidence indicates that both acute and chronic exposure to air pollution can affect COVID-19 epidemiology. The evidence is unclear for acute exposure due to a higher level of bias in existing studies as compared to moderate evidence with chronic exposure. Public health interventions that help minimize anthropogenic pollutant source and socio-economic injustice/disparities may reduce the planetary threat posed by both COVID-19 and air pollution pandemics.


2021 ◽  
pp. 1-9
Author(s):  
Ankur A. Dashputre ◽  
Keiichi Sumida ◽  
Fridtjof Thomas ◽  
Justin Gatwood ◽  
Oguz Akbilgic ◽  
...  

<b><i>Introduction:</i></b> Hypo- and hyperkalemia are associated with a higher risk of ischemic stroke. However, this association has not been examined in an advanced chronic kidney disease (CKD) population. <b><i>Methods:</i></b> From among 102,477 US veterans transitioning to dialysis between 2007 and 2015, 21,357 patients with 2 pre-dialysis outpatient estimated glomerular filtration rates &#x3c;30 mL/min/1.73 m<sup>2</sup> 90–365 days apart and at least 1 potassium (K) each in the baseline and follow-up period were identified. We separately examined the association of both baseline time-averaged K (chronic exposure) and time-updated K (acute exposure) treated as categorized (hypokalemia [K &#x3c;3.5 mEq/L] and hyperkalemia [K &#x3e;5.5 mEq/L] vs. referent [3.5–5.5 mEq/L]) and continuous exposure with time to the first ischemic stroke event prior to dialysis initiation using multivariable-adjusted Cox regression models. <b><i>Results:</i></b> A total of 2,638 (12.4%) ischemic stroke events (crude event rate 41.9 per 1,000 patient years; 95% confidence interval [CI] 40.4–43.6) over a median (Q<sub>1</sub>–Q<sub>3</sub>) follow-up time of 2.56 (1.59–3.89) years were observed. The baseline time-averaged K category of hypokalemia (adjusted hazard ratio [aHR], 95% CI: 1.35, 1.01–1.81) was marginally associated with a significantly higher risk of ischemic stroke. However, time-updated hyperkalemia was associated with a significantly lower risk of ischemic stroke (aHR, 95% CI: 0.82, 0.68–0.98). The exposure-outcome relationship remained consistent when using continuous K levels for both the exposures. <b><i>Discussion/Conclusion:</i></b> In patients with advanced CKD, hypokalemia (chronic exposure) was associated with a higher risk of ischemic stroke, whereas hyperkalemia (acute exposure) was associated with a lower risk of ischemic stroke. Further studies in this population are needed to explore the mechanisms underlying these associations.


Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 291
Author(s):  
Rossalin Yonpiam ◽  
Jair Gobbet ◽  
Ashok Jadhav ◽  
Kaushik Desai ◽  
Barry Blakley ◽  
...  

Ergotism is a common and increasing problem in Saskatchewan’s livestock. Chronic exposure to low concentrations of ergot alkaloids is known to cause severe arterial vasoconstriction and gangrene through the activation of adrenergic and serotonergic receptors on vascular smooth muscles. The acute vascular effects of a single oral dose with high-level exposure to ergot alkaloids remain unknown and are examined in this study. This study had two main objectives; the first was to evaluate the role of α1-adrenergic receptors in mediating the acute vasocontractile response after single-dose exposure in sheep. The second was to examine whether terazosin (TE) could abolish the vascular contractile effects of ergot alkaloids. Twelve adult female sheep were randomly placed into control and exposure groups (n = 6/group). Ergot sclerotia were collected and finely ground. The concentrations of six ergot alkaloids (ergocornine, ergocristine, ergocryptine, ergometrine, ergosine, and ergotamine) were determined using HPLC/MS at Prairie Diagnostic Services Inc., (Saskatoon, SK, Canada). Each ewe within the treatment group received a single oral treatment of ground ergot sclerotia at a dose of 600 µg/kg BW (total ergot) while each ewe in the control group received water. Animals were euthanized 12 h after the treatment, and the pedal artery (dorsal metatarsal III artery) from the left hind limb from each animal was carefully dissected and mounted in an isolated tissue bath. The vascular contractile response to phenylephrine (PE) (α1-adrenergic agonist) was compared between the two groups before and after TE (α1-adrenergic antagonist) treatment. Acute exposure to ergot alkaloids resulted in a 38% increase in vascular sensitivity to PE compared to control (Ctl EC50 = 1.74 × 10−6 M; Exp EC50 = 1.079 × 10−6 M, p = 0.046). TE treatment resulted in a significant dose-dependent increase in EC50 in both exposure and control groups (p < 0.05 for all treatments). Surprisingly, TE effect was significantly more pronounced in the ergot exposed group compared to the control group at two of the three concentrations of TE (TE 30 nM, p = 0.36; TE 100 nM, p < 0.001; TE 300 nM, p < 0.001). Similar to chronic exposure, acute exposure to ergot alkaloids results in increased vascular sensitivity to PE. TE is a more potent dose-dependent antagonist for the PE contractile response in sheep exposed to ergot compared to the control group. This study may indicate that the dry gangrene seen in sheep, and likely other species, might be related to the activation of α1-adrenergic receptor. This effect may be reversed using TE, especially at early stages of the disease before cell death occurs. This study may also indicate that acute-single dose exposure scenario may be useful in the study of vascular effects of ergot alkaloids.


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