Rodenticide Research Articles

THE ANTIOXIDANT PROTECTION SYSTEM STATE OF RATS UNDER EXPERIMENTAL DOXORUBICIN INTOXICATION AND THE EFFECTS OF CORRECTING FACTORS

Introduction. The doxorubicin model was used for research, which, according to many authors, most adequately reproduces heart failure of varying degrees of severity. Doxorubicin is an antibiotic that has a cytostatic effect. The mechanism of its action consists of interaction with DNA, formation of free radicals, and inhibition of nucleic acid synthesis. The doxorubicin action and the development of hypoxia are accompanied by the activation of oxidative stress, the strengthening of free radical processes, and changes in the metabolism of carbohydrates, proteins, and lipids.
 The aim of the study – the effect of the drug “Bendamine” on the indicators of antioxidant protection of the body of rats under experimental simulation of heart failure.
 Research Methods. Modeling of heart failure was performed on sexually mature male Wistar rats with a body weight of 180–200 g. In blood and myocardial homogenate, the level of lipid peroxidation products, the activity of antioxidant enzymes, and the level of reduced glutathione were determined against the background of doxorubicin intoxication and when using the drug “Bendamine”.
 Results and Discussion. During doxorubicin intoxication, LPO processes are enhanced in rats, which is indicated by the increased lipid hydroperoxides, diene conjugates, and TBA-active products in the blood and the homogenate of the rat myocardium of the first experimental group. It is worth noting that the inhibition of the antioxidant defense system was also established in intoxicated rats, as indicated by the low level of both enzymatic and non-enzymatic links of the antioxidant system. It was established that bendamine has a corrective effect on rats' oxidative stress conditions inherent in doxorubicin-induced heart failure. The drug “Bendamine” inhibits the excessive formation of POL products in pathologically changed tissues of the heart of rats and has an inducing effect on the system of antioxidant protection.
 Conclusions. The influence of the drug "Bendamine" on the indicators of antioxidant protection of the body of rats under experimental simulation of heart failure was studied. Its antioxidant properties have been proven.
 
 

Determination of acute toxicity indicators of AQUAdez-NUK 5

Currently, there is a problem in satisfying livestock enterprises with cheap, highly effective disinfectants. Import substitution of the vacated market segment requires optimization of the increasing costs of livestock companies. In this regard, preclinical studies of the AKVAdez-NUK 5 disinfectant were developed and studied, in particular, indicators of acute toxicity. In the experiment, males of the Wistar breed weighing 220-230 g were used, to whom the test solution was injected intragastrically, using a pin-shaped needle, in doses of 2000, 3000, 4000 and 5500 mg/kg. Using of analytical and statistical tools in data processing allowed us to state that for the disinfectant AQUAdez-NUK 5 has followed levels for lethal doses. LD16=2864,91mg/kg; LD50=3676,22±347,37mg/kg; standard error for LD50 is 347,37 mg/kg; LD84=4585,86 mg/kg; LD99=5040.69 mg/kg. The clinical picture of acute poisoning in rats was manifested by short-term excitement, followed by depression. Tachypnea, nasal discharge, impaired coordination of movement and clonic-tonic seizures were diagnosed in laboratory animals. The rats huddled in groups. The death of animals occurred due to respiratory arrest. By analyzing the results of an acute experiment and recording the frequency of animal deaths by observation days, the average time of animal death was calculated, which was 55.92 hours. Taking into consideration of the results, we can conclude increasing in the administered dose of the drug accelerates the onset of death of a laboratory animal. Up to the level of 4000 mg / kg, only one experimental rat died on the third day after the introduction of 3000 mg / kg. With the introduction of large dosages, lethality increased sharply, reaching 100% with the introduction of 5500 mg of AQUAdez‑NUC 5 per 1 kg of weight. In accordance with the classification of AQUAdez‑NUC 5, it can be attributed to drugs of an acute type of action with a moderate ability to cumulate. According to government standard 12.1.007-76, AQUAdez-NUK 5 belongs to hazard class III (moderately hazardous compounds).

Optimal Reference Genes for RT-qPCR Experiments in Hippocampus and Cortex of Rats Chronically Exposed to Excessive Fluoride.

Normalization of the quantitative real-time PCR (RT-qPCR) data to the stably expressed reference genes is critically important for obtaining reliable results. However, all previous studies focused on F- toxicity for brain tissues used a single, non-validated reference gene, what might be a cause of contradictory or false results. The present study was designed to analyze the expression of a series of reference genes to select optimal ones for RT-qPCR analysis in cortex and hippocampus of rats chronically exposed to excessive fluoride (F-) amounts. Six-week-old male Wistar rats randomly assigned to four groups consumed regular tap water with 0.4 (control), 5, 20, and 50 ppm F- (NaF) for 12 months. The expression of six genes (Gapdh, Pgk1, Eef1a1, Ppia, Tbp, Helz) was compared by RT-qPCR in brain tissues from control and F--exposed animals. The stability of candidate reference genes was evaluated by coefficient of variation (CV) analysis and RefFinder online program summarizing the results of four well-acknowledged statistical methods (Delta-Ct, BestKeeper, NormFinder, and GeNorm). In spite of some discrepancies in gene ranking between these algorisms, Pgk1, Eef1a1, and Ppia were found to be most valid in cortex, while Ppia, Eef1a1, and Helz showed the greatest expression stability in hippocampus. Tbp and Helz were identified as the least stable genes in cortex, whereas Gapdh and Tbp are unsuitable for hippocampus. These data indicate that reliable mRNA quantification in the cortex and hippocampus of F--poisoned rats is possible using normalization to geometric mean of Pgk1+Eef1a1 or Ppia+Eef1a1 expression, respectively.

Neuroprotective Effect of Vitamin D on Behavioral and Oxidative Parameters of Male and Female Adult Wistar Rats Exposed to Mancozeb (manganese/zinc ethylene bis-dithiocarbamate)

The constant exposure of rural workers to pesticides is a serious public health problem. Mancozeb (MZ)is a pesticide linked to hormonal, behavioral, genetic, and neurodegenerative effects, mainly related to oxidative stress. Vitamin D is a promising molecule that acts as a protector against brain aging. This study aimed to evaluate the neuroprotective role of vitamin D in adult male and female Wistar rats exposed to MZ. Animals received 40mg/kg of MZ i.p. and 12.5μg/kg or 25μg/kg vitamin D by gavage, twice a week, for 6weeks. The concentration of manganese had a significant increase in the hippocampus of both sexes and in the striatum of females, unlike zinc, which did not show a significant increase. MZ poisoning led to mitochondrial changes in brain tissues and promoted anxiogenic effects, especially in females. Alterations in antioxidant enzymes, mainly in the catalase activity were observed in intoxicated rats. Taken together, our results showed that exposure to MZ leads to the accumulation of manganese in brain tissues, and the behavior and metabolic/oxidative impairment were different between the sexes. Furthermore, the administration of Vitamin D was effective in preventing the damage caused by the pesticide.

Methemoglobin-albumin clusters for cyanide detoxification

Sodium nitrite (NaNO2) is a universal antidote for patients with cyanide poisoning. However, its use has serious drawbacks in terms of efficacy and safety. Herein, we present a promising antidote: methemoglobin (metHb)-albumin clusters. The metHb-albumin cluster is made by a metHb core wrapped by covalently bound human serum albumin. Spectral analyses proved that the metHb-albumin clusters possessed cyanide-binding properties similar to those of naked metHb. In vitro cell experiments showed that metHb-albumin clusters prevented the cyanide-induced inhibition of cytochrome c oxidase activity, resulting in a strong cytoprotective effect. In mice subjected to cyanide poisoning, metHb-albumin clusters reduced mortality and alleviated metabolic acidosis, while maintaining the activity of cytochrome c oxidase in organs; their efficacy was better than that of NaNO2. Furthermore, the oxygen carrying capacity was maintained in poisoned mice treated with metHb-albumin clusters and was low in those treated with NaNO2. These results indicate that metHb-albumin clusters could be a more effective and safer antidote against cyanide poisoning than NaNO2.

Penetrating the Blood-Brain Barrier for Targeted Treatment of Neurotoxicant Poisoning by Nanosustained-Released 2-PAM@VB1-MIL-101-NH2(Fe).

It is very important to establish a sustained-release pralidoxime chloride (2-PAM) drug system with brain targeting function for the treatment of neurotoxicant poisoning. Herein, Vitamin B1 (VB1), also known as thiamine, which can specifically bind to the thiamine transporter on the surface of the blood-brain barrier, was incorporated onto the surface of MIL-101-NH2(Fe) nanoparticles with a size of ∼100 nm. Pralidoxime chloride was further loaded within the interior of the above resulted composite by soaking, and a resulting composite drug (denoted as 2-PAM@VB1-MIL-101-NH2(Fe)) with a loading capacity of 14.8% (wt) was obtained. The results showed that the drug release rate of the composite drug was increased in PBS solution with the increase of pH (2-7.4) and a maximum drug release rate of 77.5% at pH 4. Experiments on the treatment of poisoning by gavage with the nerve agent sarin in mice combined with atropine revealed that sustained release of 2-PAM from the composite drug was achieved for more than 72 h. Sustained and stable reactivation of poisoned acetylcholinesterase (AChE) was observed with an enzyme reactivation rate of 42.7% in the ocular blood samples at 72 h. By using both zebrafish brain and mouse brain as models, we found that the composite drug could effectively cross the blood-brain barrier and restore the AChE activity in the brain of poisoned mice. The composite drug is expected to be a stable therapeutic drug with brain targeting and prolonged drug release properties for nerve agent intoxication in the middle and late stages of treatment.

Suicidal crisis in the adolescent: About 3 clinical cases

IntroductionSuicide is the third most common cause of death among adolescents. It is linked to several mental pathologies. Early detection and effective and rapid management are essential elements to improve the mental health of the adolescent and prevent suicidal behaviour.ObjectivesOur objective is :-To discuss through these medical observations the risk factors and pathologies at high risk of suicide,-To detail the urgent course of action to be taken in the event of suicide attempts and-To underline the importance of early management to prevent suicide in adolescentsMethodsWe report hereafter the clinical cases of 3 adolescents followed in child psychiatry for the management of a suicidal crisis.Results1st clinical case :This is a 13 year old girl, brought back by the staff of the Lalla Meryem child protection centre, where she has been living since her separation from her family following abuse by her mother. She reports a reliving of scenes where her mother burned her private parts. She reports disturbed sleep with night terrors and nightmares. In addition, the centre’s staff reported irritability, crying spells and verbalized suicidal threats.2nd clinical case:This is a 15 year old girl referred by the paediatric service for management of a suicide attempt by ingestion of rat poison. She stopped her schooling 2 years ago to take care of her mother who had cervical cancer and died 6 months ago. Since then, she has experienced sadness of mood, low self-esteem with ideas of devaluation. During the first psychiatric interview, she did not criticize her suicidal act and said that she wanted to kill herself, which she considered the only solution to her suffering.3rd clinical case:This is a 12-year-old adolescent, followed in child psychiatry for conduct disorder with problematic use of tobacco, cannabis and benzodiazepines. He had stopped going to school since the third grade.He consulted for a suicide attempt by ingesting 30 antihypertensive tablets. After somatic care, he was referred to us from the medical emergency department for psychiatric care.ConclusionsSuicide among adolescents is on the increase in Morocco. It is necessary to take into account the risk of suicide in the face of any mental or somatic pathology. A rapid and urgent course of action is necessary to avoid recurrence.Disclosure of InterestNone Declared

A synthetic porphyrin as an effective dual antidote against carbon monoxide and cyanide poisoning

Simultaneous poisoning by carbon monoxide (CO) and hydrogen cyanide is the major cause of mortality in fire gas accidents. Here, we report on the invention of an injectable antidote against CO and cyanide (CN-) mixed poisoning. The solution contains four compounds: iron(III)porphyrin (FeIIITPPS, F), two methyl-β-cyclodextrin (CD) dimers linked by pyridine (Py3CD, P) and imidazole (Im3CD, I), and a reducing agent (Na2S2O4, S). When these compounds are dissolved in saline, the solution contains two synthetic heme models including a complex of F with P (hemoCD-P) and another one of F with I (hemoCD-I), both in their iron(II) state. hemoCD-P is stable in its iron(II) state and captures CO more strongly than native hemoproteins, while hemoCD-I is readily autoxidized to its iron(III) state to scavenge CN- once injected into blood circulation. The mixed solution (hemoCD-Twins) exhibited remarkable protective effects against acute CO and CN- mixed poisoning in mice (~85% survival vs. 0% controls). In a model using rats, exposure to CO and CN- resulted in a significant decrease in heart rate and blood pressure, which were restored by hemoCD-Twins in association with decreased CO and CN- levels in blood. Pharmacokinetic data revealed a fast urinary excretion of hemoCD-Twins with an elimination half-life of 47 min. Finally, to simulate a fire accident and translate our findings to a real-life scenario, we confirmed that combustion gas from acrylic cloth caused severe toxicity to mice and that injection of hemoCD-Twins significantly improved the survival rate, leading to a rapid recovery from the physical incapacitation.

Infrared spectroscopy and biochemical parameters of rat tissues under heavy metal poisoning conditions

The increasing level of anthropogenic environmental pollution and effective means to reduce the negative impact of xenobiotics on animal and human health is an urgent problem today. Considering this, the purpose of the study is to examine the effect of heavy metals on accumulation processes under poisoning conditions, and biochemical parameters in the body of rats. Analogue groups were formed of rats of the same age, gender, and body weight to conduct the study. Rats were poisoned with solutions of copper sulfate, zinc sulfate, cadmium sulfate, and lead nitrate for 14 days. Using the method of infrared spectroscopy, substantial differences in the spatial structure of protein components in intact and poisoned animals were established. The difference between the spectral characteristics of the examined tissues is clearly demonstrated by the statistical indicators of skewness and kurtosis. It was determined that poisoning of rats with copper, zinc, cadmium, and lead ions affects the course of glycolysis reactions and the tricarboxylic acid cycle, which leads to a likely increase in serum concentrations of lactate and pyruvate, oxaloacetate and α-ketoglutarate and a decrease in Malate content compared to intact rats. It was established that under the conditions of poisoning, there is also a substantial increase (P < 0.05) in the content of the examined heavy metals in the blood, liver, and kidneys. In animals poisoned with heavy metals, a decrease in the pool of free amino acids in the kidneys is observed. In particular, the content of aspartic acid, valine, glycine, tyrosine, and cystine (more than 1.5 times) in the kidneys of such rats decreases; alanine, leucine, serine, taurine, threonine, phenylalanine (more than 2.0 times), lysine – 3.4-4.9 times. Therewith, an increase in the level of isoleucine and methionine by 1.3-1.5 times, ornithine – by 1.8-2.1 times, and glutamic acid – by 4.4-5.3 times in rats of the experimental group compared to intact ones was identified. The results of the study can be helpful in the professional activities of doctors of veterinary medicine, toxicologists, biologists, and environmentalists and used to control the quality of livestock products, conduct toxicological studies, and analyse environmental objects

Evaluation of therapeutic effects of camel milk against the hepatotoxicity and nephrotoxicity induced by fipronil and lead acetate and their mixture

Elevated environmental pollution of lead and fipronil is blamed for chronic toxicity. Fipronil and lead acetate are commonly used, but now no adequate data is available concerning the harmful side effects of their mixture. The present work investigated the curative effects of camel milk against lead and fipronil subchronic toxicity individually and as mixture with different doses (1/30 and 1/60 LD50) on male albino rats by oral ingestion. Rats were divided into eight groups; the first group (G1) was the normal health control. G2, G4, G6, and G8 are the normal health groups camel milk. G3 and G4 are ingested by 1/30 LD50 of the fipronil formulation. G5 and G6 are ingested by 1/30 LD50 of lead acetate. G7 and G8 are ingested by 1/60 LD50 of lead acetate and 1/60 LD50 of fipronil formulation. The lead acetate or fipronil and their mixture significantly induced destructive damage to the kidneys and liver function parameters as well as lipid profile and oxidative stress in both organs. Serum LDH activity increased under the same conditions. Most harmful effects were clearly observed in G7 followed by G3 and G5. Histological examination revealed hepatic degeneration and nephropathy in intoxicated rats relative to normal health control, as shown by hypertrophy of hepatocytes in addition to karyomegaly, binucleation, and mild individual cell coagulative and mild hypertrophy, as well as a vacuolar degeneration of tubular epithelium in the kidneys. Both toxicants in their mixture showed more harmful than those of their individual ones. Camel milk treatments into intoxicated animals (lead, fipronil, and mixture groups) attenuated all evaluated parameters, alleviated the harmful influences of the mixture of lead acetate and fipronil, and improved the biomarkers of their oxidative stress.

Attenuation of fluoride-induced hepatorenal oxidative stress by ferulic acid in vivo: An approach with in-silico analysis and interaction informatics of ferulic acid

BackgroundChronic fluoride toxicity induces oxidative strain and lipid peroxidation and imparts deleterious effects on human metabolic organs. AimThe present study aimed to expose the defensive impact of ferulic acid against sodium fluoride (NaF) induced hepatorenal dysfunction at the biochemical and antioxidative systems. MethodsIn-vivo. Rats were arbitrarily separated into five groups as control, sodium fluoride-treated (200 ppm kg −1), vitamin C -as a positive control, and FA co-administered groups with 10 mg kg −1 and 20 mg kg −1 body weight for 56 days. In the present investigation, we measured antioxidant enzymes, superoxide dismutase, catalase, and lactate dehydrogenase by electrozymographic and spectrophotometric methods. Biochemical assessment of TBARS, conjugated diene, and different serum biomarkers was done for liver and kidney functionality tests.In-silico. An in-silico study was conducted through a molecular docking experiment to evaluate the binding potentiality of FA by employing AutoDock Vina [version 1.5.6] to overcome the abnormality in the activities of catalase, and superoxide dismutase in NaF promoted toxicity of hepatorenal system.In-vitro. An in vitro biochemical experiment was conducted to support the in-silico study. ResultsSuperoxide dismutase and catalase were decreased in the intoxicated rat. Ferulic acid (FA) as an antioxidant remarkably defended the NaF-mediated deterioration of the antioxidative status in the hepatorenal system, lowering lipid peroxidation products, malondialdehyde, and conjugated diene. Serum biomarkers, ALT, AST, ALP, urea, and creatinine increased in the intoxicated group than in control. Ferulic acid significantly neutralized the ill effects of NaF on serum lipid profile. In-silico analysis hypothesized the strong interaction of FA with the active side of catalase and superoxide dismutase that prevented the binding of NaF at the active site of these mentioned enzymes and this was further validated by in-vitro assay. ConclusionHowever, FA modulates free radical generation and protected these metabolic organs against sodium fluoride-induced injury.

Liver Transplant in an Unusual Case of Acute Fulminant Hepatic Failure: A Case Report

Yellow phosphorus ingestion causing acute fulminant hepatic failure is a serious condition. The establishment of health measures to monitor and prevent yellow phosphorus poisoning is of utmost importance because there is no known cure for the condition. To prevent phosphorus poisoning, it is crucial to raise awareness among the general population about its potential fatality, educate primary care physicians about the delayed onset toxidrome, and take precautions to ensure careful monitoring and reporting. Herein, we present a case of case of a 33-year-old male who consumed 30 grams of rat poison {Yellow Phosphorus (YP)} while under the influence of alcohol. He presented to us on day 5 with icterus and bilateral subconjunctival haemorrhage. Laboratory investigations revealed severely deranged liver function tests and raised Prothrombin Time (PT)/International Normalised Ratio (INR), indicating acute fulminant hepatic failure. The patient was started on N-acetyl cysteine, vitamin K, and received fresh frozen plasma transfusion. Despite treatment, on day 3, the patient developed grade 4 Hepatic Encephalopathy (HE) and the laboratory parameters worsened. Close monitoring revealed further deterioration, leading to the decision for emergency orthotopic Liver Transplantation (LT) on day 7. Following the transplant, the patient's liver function tests showed improvement. The subconjunctival haemorrhage and icterus resolved completely on day 3 post-transplantation. The patient was extubated on day 3 and discharged on day 5 post-transplantation. Regular follow-up appointments were uneventful. In conclusion, the present case report highlights the successful management of a patient with acute fulminant hepatic failure through early hepatic transplantation. It emphasizes the importance of prompt recognition, appropriate treatment, and timely transplantation in improving patient outcomes.

PECTIN MODULATES HEMATO-BIOCHEMICAL PARAMETER, HISTOPATHOLOGY, OXIDATIVE STRESS BIOMARKERS, CYTOKINES AND EXPRESSION OF HEPCIDN GENE IN LEAD INTOXICATED RATS

Publications concerning the protective effect of pectin against lead induced toxicity in rats are not available. In order to study such effect, 40 male rats were divided into 3 groups. The first group was contained 10 rats that kept as control group. The second group was contained 10 rats that received pectin at dose of 100 mg/kg BW during experimental period (8 weeks). The third group was contained 20 rats that received 400mg/kg BW of lead acetate daily for 4 weeks then divided into two subgroups (3A and 3B). Subgroup 3A contained 10 rats that still receive lead acetate in the same dosage whereas, subgroup B co-treated with lead acetate and pectin daily for another 4 weeks. Blood samples were collected after 2, 4 and 8 weeks from the start of the experiment. Liver, kidney and bone marrows were collected only at the end of the experiment. Lead acetate induced anemia only after 4 weeks of administration as reflected on decreased values of Hb, PCV, MCV, MCH and MCHC. These indices remained at lower levels in lead acetate treated groups until the end of the experiment. Concentrations of serum ferritin, iron, total antioxidant capacity (TAC) and reduced glutathione (GSH) and the expression of hepatic hepcidin gene were decreased significantly in lead acetate intoxicated rats compared to control. Activities of ALT and AST and concentrations of urea, creatinine, Nitric oxide (NO), TNF-α, IL-6, total iron binding capacity (TIBC) and lead were increased significantly in lead acetate intoxicated group compared to control. Hepatic degeneration and hemorrhage, renal lytic necrosis and apoptosis of myeloid cells were most prominent changes in lead intoxicated rats. Lead acetated related changes were improved by co-treatment with pectin however; normal control values have not been achieved. Conclusively, pectin is recommended to protect against lead acetate toxicity in rats. Key words: lead acetate; toxicity; pectin; hepcidin; oxidative stress biomarkers; histopathology

Study of parameters of lipid peroxidation and antioxidant protection in rats treated with cadmium nitrate with biocorrection by infusion of Beta vulgaris seeds

Recently, interest in natural antioxidants and their use in the food industry has increased. In addition to ensuring maximum safety of the produced product, they also serve as an antioxidant shield for the entire living organism. Plant extracts contain flavonoid compounds that have an antioxidant effect. In this regard, the purpose of the article is to study the antioxidant properties of infusion of Beta vulgaris’s seeds, to establish the relationship between acute and subacute inoculation of rats with cadmium nitrate and oxidative stress. For this experimental study, we used 50 male rats. The animals were exposed to Cd nitrate, with an initial weight of 180 ± 30 g. The first groups of rats were injected with cadmium nitrate at a dose of 0.1 g/L inter peritoneal, the second groups received a 0.01% solution of cadmium nitrate 1 ml 5 days a week, orally for 10 and 24 days. The state of oxidative metabolism in the blood was investigated. To assess the state of oxidative metabolism in the blood, the primary, secondary and end products of lipid peroxidation were determined, such as diene conjugates (DC), cetodiene (CD), malondialdehyde (MDA), Schiff bases (SHB), and the activity of glutathione peroxidase (GP), catalase (CAT), and adenosine deaminase (ADA) enzymes were evaluated by the parameters of antioxidant protection. The mean ± SEM values were calculated for each group to determine the significance of the intergroup difference. Each parameter was analyzed separately using the one-way analysis of variance (ANOVA) test. To determine the difference between groups, Student’s “t”-test was used. Studies have shown that with the use of cadmium in the blood of experimental animals, there is a violation of catabolits of lipoperoxidation, depending on the length of the days of poisoning, but a significant decrease in the biocorrection of Beta vulgaris’s seeds. Because of in this study, we found that the activity levels of antioxidant defense enzymes were significantly increased in the blood of experimental animals, which biocorrected with beetroot seed infusion. In conclusion, our study allows us to state that the use infusion of Beta vulgaris’s seeds in subacute and acute experiments with poisoning of experimental rats with cadmium nitrate as an antioxidant protective effect.

Effects of Two Months Durational Vitamin E Therapy on Paraquat-inflicted Liver Damage in Wistar Rats (Rattus norvegicus)

Paraquat is a highly poisonous chemical that is commonly used as a herbicide (plant killer) to control weeds and grasses. It has been found to disrupt the levels and activities of some liver enzyme parameters. This experimental study was aimed at assessing the effect of Vitamin E in restoring liver physiology in paraquat-induced liver poisoning in rats. In this study, 200 male rats with a mean weight of 0.20.02kg, with 50 rats in each group of four, labeled A, B, C, and D. The "A" group received no paraquat, while the "B", "C", and "D" groups received 0.02g, 0.04g, and 0.06g of paraquat per kilogram of rat every two weeks for three months respectively. Each group also had a subgroup treated only with vitamin E and the Vit. E + paraquat subgroup BVE, CVE, and DVE but AVE was treated with paraquat but only Vit E. The blood was taken and the liver function was assayed. The result showed that there was a significant dose-dependent increase (P-value<0.05) in the levels liver enzymes in the subgroups treated with paraquat alone (A0, B0, C0 and D0). After treatment with vit E, the result revealed that there a significant decrease (P-value<0.05) in the level of the liver enzymes when compared to the corresponding subgroups without Vit. E treatment. This study has shown that vit E can ameliorate the effect of paraquat liver poisoning particularly when the treatment is administered weekly for two months.

The potential mechanism of histamine-inducing cardiopulmonary inflammation and apoptosis in a novel oral model of rat intoxication

Histamine (HIS) is a potent vasodilator that contributes to anaphylactic reactions. Our investigation aims to study the possible toxic impact of repeated oral administration of histamine on the target organs of HIS poisoning (lung & heart) in rats as a model of scombroid poisoning. We used 15 rats that were separated into three groups with 5 rats in each. All rats received the treatments orally for 14 days as follows; (1): distilled water, (2) HIS at a dosage level of 250 mg/kg BWT daily and (3) HIS at a dosage level of 1750 mg/kg BWT weekly. Our results revealed that the consumption of HIS either daily or weekly could cause marked cardiopulmonary toxicity in rats. HIS can trigger inflammatory reactions in the cardiopulmonary tissues and induce oxidative stress damage along with apoptosis of such organs. HIS was markedly increase the MDA levels and decrease the CAT and GSH activity in both lung and heart tissues. The main pathological lesion observed is inflammation which was confirmed by immunohistochemistry and demonstrated strong iNOS and TNF-α protein expressions. Cardiac muscles showed extensive degeneration and necrosis and displayed strong casp-3 protein expression. Additionally, all HIS receiving groups noticed marked elevation of the pulmonary transcription levels of Cox2, TNF-α, and IL1β along with substantial elevation of casp-3 and bax genes and downregulation of Bcl2 gene in the cardiac tissue. We concluded that the oral administration of HIS either daily or weekly can induce cardiopulmonary toxicity via the upregulation of proinflammatory cytokines resulting in ROS overgeneration and inducing both oxidative stress and apoptosis.

Ulva fasciata, a green alga, attenuates the kidney and liver dysfunctions in rats induced by acetaminophen

Acetaminophen (AAP) is an analgesic–antipyretic drug which is considered safe at recommended dose, but its overuse may induce renal and hepatic injuries. Marine macro algae have great potential against drug-induced renal and hepatic dysfunctions. The present study described the reno-protective and hepato-protective effects of the ethanol extract of an edible green alga Ulva fasciata and its fractions (n-hexane, chloroform and methanol) against AAP toxicity. In the 1st set of experiment, rats were divided into five groups. Of which two were treatment groups beside three controls, the first treatment group was given ethanol extract of U. fasciata alone and the second group was given the same extract with AAP. In the 2nd set of experiment, rats were divided into nine groups, of which three treatment groups administered n-hexane, chloroform and methanol fractions of ethanol extract of U. fasciata respectively while other three treatment groups received the same fractions individually with AAP. On the 11th day, rats were decapitated after 12 h of fasting from both sets, blood samples were collected for assessment of biochemical parameters and kidney tissues were used for determination of oxidants and antioxidants. Histopathological assessment was also done in kidney tissues. A single dose of AAP (600 mg/kg) affected kidney markers including creatinine, urea and blood urea nitrogen (BUN) and hepatic enzymes. Ethanolic extract of U. fasciata normalized kidney and liver markers in AAP intoxicated rats. AAP also reduced glutathione (GSH) in kidney tissues and altered kidney architecture, which were improved by ethanolic extract and chloroform soluble fraction of U. fasciata. A total of 14 polyunsaturated fatty acids were identified from chloroform soluble fraction of U. fasciata by GC-MS and assumed these may be involved in protective activities of U. fasciata.

Effects of Ozone Therapy on Chronic Arsenic Poisoning in Rats.

Arsenic (As) is a toxic metalloid that affects many organs through drinking water. This study aims to examine the efficacy of ozone therapy on chronic arsenic toxicity. Twenty-four male Wistar albino rats were housed in individual cages and grouped as control, As, O3, and As + O3. As was applied by adding 5mg/kg/day in drinking water for 60days. Ozone therapy was applied at 0.5mg/kg/day (i.p.) O3 in the last 5days of the experimental period. Tissues were harvested and analyzed for histopathological injury and apoptotic markers. There was no significant difference between the As + O3 and O3 groups (p = 0.186 and p = 0.599) for light microscopic criteria: inflammatory cell infiltration and hydropic degeneration in liver tissue.In TUNEL assessments, similar outcomes were obtained in the control and As + O3 groups. A statistically significant increase was observed in p53 and Caspase 3 (Casp-3) expression levels in the As group compared to the O3 and As + O3 groups. There was no significant difference between the As + O3 and O3 groups on peritubular hemorrhage and desquamation parameters in kidneys (p = 0.147 and p = 0.094). The KIM-1 expression level was significantly increased in the As group compared to the As + O3 group (p = 0.01), and the Casp-3 expression level was not significantly changed in the O3 group compared to the As + O3 group (p = 0.59). In conclusion, it is determined that ozone therapy has ameliorative effects on the microscopic injury of liver and kidney tissues. In addition to microscopic improvement, KIM-1 gene expression levels were ameliorated in the kidneys. The apoptotic cell counts and the Casp-3 and p53 gene expression levels were decreased by O3 administration. Thus, ozone therapy can be a treatment choice for As toxicity.

Neuroprotective effect of Foeniculum vulgare essential oil in developing Wistar rats exposed to manganese chloride

The present study was carried out in order to evaluate, on the one hand, the modifications induced by manganese chloride according to a neurobehavioral, biochemical and histological approach in developing Wistar rats and, on the other hand, to test the effectiveness of Foeniculum vulgare (fennel) essential oil (FEO) in restoring or not the harmful effects of manganese chloride (MnCl2). The characterization of this essential oil by gas chromatography showed that the major component is E-anethole (34.7907%). The administration of FEO corrected the depressive state, anxiety and locomotor hypoactivity respectively observed in rats exposed to MnCl2, thus, the FEO restored the activity of the various antioxidant enzymes with a clear improvement of the cerebral tissue architecture in intoxicated rats treated with FEO. In conclusion, the FEO has a beneficial effect on the nervous system of rats intoxicated with MnCl2 which justifies the importance of this oil in traditional medicine.

Succession pattern of insects in relation to drowning and poisoning of Rattus norvegicus at Delta State University, Abraka, Southern Nigeria

Forensic study using insects is a veritable tool for tracing crime and cruelty cases. In recent times, forensics is gaining local or international attention. Poisoning and drowning are similar criminal cases occurring in Nigeria, thus, this present study determined insects associated with decaying carcasses of rats drowned and poisoned in Site III, of Delta State University, Abraka, Nigeria. Poisoned and drowned rats were positioned at several mapped spots in undeveloped bushy paths close to the uncompleted University library in replicates. Albino Wistar rats of 0.25 to 0.30kg were killed by poisoning and drowning. The carcasses were observed daily, between the hours of 8 am and 6 pm, with a minimum observation time of one hour per sample. A total of 1318 insect belonging to 3 Orders, 6 Families and 7 insect species was encountered in this study. Musca domestica, Sarcophaga albiceps and Calliphora viciniam were common species associated with poisoning and drowning of rats. Six hundred and eighty-nine (689) insects accounting for 52.3% was recovered from drowned rats while poisoned rats accounted for (12.37%) of insect species as compared to control (35.36%). The differences were significant (p < 0.05). More insects were collected during the decay stage of the drowned carcass (53.17%). The overall duration for decomposition was not significantly faster (F= 0.89, p > 0.05) for drowned carcass (mean ± SD= 21.43 ± 9.10 days) in poisoned carcass (mean ± SD= 9.53 ± 1.75 days) and control (mean ± SD= 13.21 ±2.20 days). The results of this present study have shown that poisoning inhibited insect abundance. The occurrence of dipterans in all stages is an indication that they can be adopted as key species to determining poison and drowned carcasses. Though future studies are required studies to confirm this is required to develop the succession status in forensic entomology studies using other animal models.