Cellular Damage After Prolonged Low-Dose Exposure of Neonicotinoid in Rats

Abstract Background; Dinotefuran is a new class of neonicotinoids claimed to be harmless to mammals and humans. This claim was daunted by the documented effect of dinotefuran on honeybees and further studies were required. Aim: The study was designed to assess the capaciousness of damage caused by prolonged exposure of dinotefuran in mammals and probable strategy to neutralize its effect. Methodology: Ninety-day trial using Wistar rats (n=45) was conducted while dividing them into three groups: untreated control group, insecticide (dinotefuran) treated group, and dinotefuran treated and vitamin E supplemented group. Dinotefuran was administrated orally (LD25). Vitamin E (alpha-tocopherol) supplementation was given in water ad libitum. Blood sampling was done twice a month, and hematological and biochemical data were recorded. After expiry of trial period, the experimental rats were anesthetized and sacrificed. Organs (kidneys, liver, and heart) were isolated from each groups, weighed, and stored at approximately -20°C till further processing, analysis and histopathology were performed. Results: All the hematological parameters were affected significantly. Histopathology of tissues showed clear necrosis in all the tissues except kidneys. All the biomarkers of oxidative stress and comet assay demonstrated significant cell damage. All the parameters showed improvement after vitamin E supplementation but non-significantly. Significance: These findings were suggestive that even low dose persistent exposure can lead to mutagenicity and carcinogenicity in mammals and other non-target species hence revised policy guidelines and more intelligent use of these chemicals is required.

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Comparison of the Antioxidant Nutrient Profile among Normal Pregnant Women and Women having Pregnancy Induced Hypertension

Pakistan Journal of Public Health ◽

10.32413/pjph.v10i4.388 ◽

2021 ◽

Vol 10 (4) ◽

pp. 246-251

Author(s):

Kausar Aamir ◽

Arfa Azhar ◽

Fatima Abid ◽

Shamaila Khalid ◽

Fiza Ali Khan

Keyword(s):

Vitamin E ◽

Pregnant Women ◽

Cell Damage ◽

Alpha Tocopherol ◽

Control Group ◽

P Value ◽

Pregnancy Induced Hypertension ◽

Nutrient Profile ◽

Induced Hypertension ◽

Mild Hypertensive

Background: Preeclampsia is a multifactorial disorder comprising many organs. Oxidative stress (OS) has been intensely linked to its occurrence. Vitamin E, a lipophilic chain breaking antioxidant has been proved to suppress the OS. Present study was designed to investigate antioxidant nutrient profile in patients with different grades of pregnancy induced hypertension (PIH) and to compare them with normal pregnant controls. Methods: The study group comprised 110 patients divided in three groups as Group A (n=40) Normotensive patients, Group B (n=40) Mild hypertensive, Group C (n=30) Severe hypertensive. Vitamin A, B-Carotene, serum alpha tocopherol (vitamin E) and vitamin C levels were analysed. Results: Serum alpha tocopherol (vitamin E) was significantly low in severe and mild cases (0.32±0.00 mg/dl, 0.74±0.03 mg/dl respectively), when compared with normal pregnant women levels (0.78±0.040). All other nutrients were also found to be in reduced quantity for Group C when compared to control group (P value <0.001). Conclusion: It was therefore concluded that in patients with risk of preeclampsia (PE) adequate antioxidant nutrients may have a role in cessation of free radical-mediated cell disturbances, and thereby protecting against endothelial cell damage, which is the key factor in PE development.

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BIOCHEMICAL AND HAEMATOLOGICAL BIOMARKER DETERMINED IN FEMALE ALBINO RATS INDUCED WITH INFERTILITY AND ADMINISTERED WITH ANTHOCLIESTA VOGELII

JOURNAL OF RESEARCH AND REVIEW IN SCIENCE ◽

10.36108/jrrslasu/7102/40(0182) ◽

2017 ◽

Vol 4 (1) ◽

Author(s):

Olugbenga Oladimeji ◽

O.A Lawal ◽

A Steve

Keyword(s):

Vitamin E ◽

Hematological Parameters ◽

Treated Group ◽

Female Rats ◽

Control Group ◽

Albino Rats ◽

Traditional Use ◽

Blood Samples ◽

Biochemical Evaluation ◽

Automated Hematology Analyzer

Anthocleista vogelii was investigated for the acclaimed fertility enhancing properties especially in females. The phyto-chemistry of the ethanolic leave extract of Anthocleista vogelii was determined prior to it being administered orally for 14 days to Wister albino rats. Micronor (norethisterone) or N-acetylcysteine (NAC) was given orally to induce temporary infertility in the female rats for seven (7) days prior to other treatment. The Blood samples from experimental animal groups were collected through cardiac puncture when the rats were sacrificed after the completion of fourteen (14) days extract administration. The vitamin E analysis was performed using HPLC. The hematological parameters were performed using the Sysmex® Automated Hematology Analyzer KX-21N. Biochemical evaluation of glutamic pyruvate transaminase ALT, alkaline phosphatase ALP, glutamic oxaloacetate transaminase AST, total cholesterol and total triacylglycerol was done using randox biochemical kits. The extract was found to possess Anthraquinones, Terpenoids, Flavonoids, Saponins, Alkaloids, Phenols and Phytosterols. The hematological parameters showed a significant increase (P<0.05) in absolute middle cells (basophils, eosinophils and monocytes) count. It also showed a significant reduction in the ALP, ASP, AST, TAG and cholesterol level (p<0.05). The obtained results showed a significant increase of vitamin E concentration in the female rats in the control group compared to extract treated group. The result also suggest that Anthocleista vogelii may have a role in creating the environment required for enhancing pregnancy with the Vitamin E concentration production that support the claims on the traditional use of Anthocliesta vogelii to enhance fertility in female.

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Synergistic Hepatoprotective Interaction between α-Tocopherol and Ascorbic Acid on Paracetamol Induced Liver Damage in Rats

10.20944/preprints202006.0122.v1 ◽

2020 ◽

Cited By ~ 1

Author(s):

Saidul Islam Khan ◽

Mahmuda Begum ◽

Rama Chowdhury ◽

Md. Mizanur Rahman ◽

Muhammad Asaduzzaman

Keyword(s):

Ascorbic Acid ◽

Vitamin E ◽

Liver Damage ◽

Treated Group ◽

Alpha Tocopherol ◽

Male Rats ◽

Control Group ◽

Group I ◽

Control Group Group

Background and objectives: The hepatoprotective activity of vitamin E and C is evident due to their ability of modulating the antioxidant pathway. In this study, we have evaluated the effects of α-tocopherol and ascorbic acid on paracetamol induced liver damage with offsetting various levels of drug treatment following an in vivo experimental protocol on Wistar albino male rats. Materials and Methods: The level of lipid peroxidation as well as histological examination of liver tissues were observed among 50 Wistar albino male rats to evaluate hepatoprotective effect of α-tocopherol and ascorbic acid on hepatocytes. The experiment was divided into 5 groups (10 rats in each group)- Basal control group (Group-I, with propylene glycol), Paracetamol treated control group (Group –II), α-tocopherol pretreated & paracetamol treated group (Group –III), Ascorbic acid pretreated & paracetamol treated group (Group –IV) and Ascorbic acid pretreated & paracetamol treated group (Group –IV). Results: The mean (± SD) Malondialdehyde (MDA) concentration were significantly reduced in α-tocopherol pretreated and paracetamol treated group (P<0.001), Ascorbic acid pretreated and paracetamol treated group (P≤0.05) and combined α-tocopherol with ascorbic acid pretreated & paracetamol treated group (P<0.001). Statistically significant differences in histological findings of rat liver were observed in paracetamol treated control group (P<0.001), ascorbic acid pretreated and paracetamol treated group (P<0.001). The serum alanine aminotransferase (ALT) level was also significantly higher in paracetamol treated group (P<0.001), α-tocopherol pretreated plus paracetamol treated group (P≤0.05) and in ascorbic acid pretreated plus paracetamol treated group (P<0.001). Conclusion: The combined pretreatment of α-tocopherol & ascorbic acid have better hepatoprotective effects than α-tocopherol or ascorbic acid alone against paracetamol induced liver damage. The decrement of free radicals produced by vitamin E could be a better hepatoprotective antioxidant than vitamin C in paracetamol induced toxicity.

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Vitamin E Can Ameliorate Oxidative Damage of Ovine Hepatocytes In Vitro by Regulating Genes Expression Associated with Apoptosis and Pyroptosis, but Not Ferroptosis

Molecules ◽

10.3390/molecules26154520 ◽

2021 ◽

Vol 26 (15) ◽

pp. 4520

Author(s):

Luyang Jian ◽

Ying Xue ◽

Yuefeng Gao ◽

Bo Wang ◽

Yanghua Qu ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Cell Death ◽

Vitamin E ◽

Oxidative Damage ◽

Treated Group ◽

Cellular Damage ◽

Control Group ◽

Group 4 ◽

Intracellular Ros

(1) Background: the current research was conducted to investigate the potential non-antioxidant roles of vitamin E in the protection of hepatocysts from oxidative damage. (2) Methods: primary sheep hepatocytes were cultured and exposed to 200, 400, 600, or 800 μmol/L hydrogen peroxide, while their viability was assessed using a CCK-8 kit. Then, cells were treated with 400 μmol/L hydrogen peroxide following a pretreatment with 50, 100, 200, 400, and 800 μmol/L vitamin E and their intracellular ROS levels were determined by means of the DCF-DA assay. RNA-seq, verified by qRT-PCR, was conducted thereafter: non-treated control (C1); cells treated with 400 μmol/L hydrogen peroxide (C2); and C2 plus a pretreatment with 100 μmol/L vitamin E (T1). (3) Results: the 200–800 μmol/L hydrogen peroxide caused significant cell death, while 50, 100, and 200 μmol/L vitamin E pretreatment significantly improved the survival rate of hepatocytes. ROS content in the cells pretreated with vitamin E was significantly lower than that in the control group and hydrogen-peroxide-treated group, especially in those pretreated with 100 μmol/L vitamin E. The differentially expressed genes (DEGs) concerning cell death involved in apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2), pyroptosis (NLRP3, IL-1β, and IRAK2), and ferroptosis (TFRC and PTGS2). The abundances of IL-1β, IRAK2, NLRP3, CASP8, CASP8AP2, RIPK1, and TLR7 were significantly increased in the C1 group and decreased in T1 group, while TFRC and PTGS2 were increased in T1 group. (4) Conclusions: oxidative stress induced by hydrogen peroxide caused cellular damage and death in sheep hepatocytes. Pretreatment with vitamin E effectively reduced intracellular ROS levels and protected the hepatocytes from cell death by regulating gene expression associated with apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2) and pyroptosis (NLRP3, IL-1β, and IRAK2), but not ferroptosis (TFRC and PTGS2).

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Effect of hyperglycemia on brain pH levels in areas of focal incomplete cerebral ischemia in monkeys

Journal of Neurosurgery ◽

10.3171/jns.1986.65.5.0693 ◽

1986 ◽

Vol 65 (5) ◽

pp. 693-696 ◽

Cited By ~ 46

Author(s):

W. Richard Marsh ◽

Robert E. Anderson ◽

Thoralf M. Sundt

Keyword(s):

Adverse Effect ◽

Cerebral Ischemia ◽

Cell Damage ◽

Treated Group ◽

Squirrel Monkeys ◽

Control Group ◽

Content Type ◽

Brain Ph ◽

Fine Print ◽

Incomplete Ischemia

✓ The adverse effect of a minimal cerebral blood flow (CBF) in models of global ischemia has been noted by many investigators. One factor believed important in this situation is the level of blood glucose, since a continued supply of this metabolite results in increased tissue lactate, decreased brain pH, and increased cell damage. The authors have extended these observations to a model of focal incomplete ischemia. Brain pH was measured in fasted squirrel monkeys in regions of focal incomplete ischemia after transorbital occlusion of the middle cerebral artery (MCA). In both control and hyperglycemic animals, CBF was reduced to less than 30% of baseline. At 3 hours after MCA occlusion, brain pH in the control group was 6.66 ± 0.68 as compared to 6.27 ± 0.26 in the glucose-treated group. This difference was statistically significant by Student's unpaired t-test (p < 0.05). Thus, hyperglycemia results in decreased tissue pH in regions of focal incomplete cerebral ischemia in monkeys.

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Effects of Vitamin E and Vitamin C on Mercury Induced Toxicity in Mice

Progressive Agriculture ◽

10.3329/pa.v19i2.16949 ◽

2013 ◽

Vol 19 (2) ◽

pp. 93-100 ◽

Cited By ~ 3

Author(s):

MA Huq ◽

MA Awal ◽

M Mostofa ◽

A Ghosh ◽

AR Das

Keyword(s):

Body Weight ◽

Vitamin E ◽

Vitamin C ◽

Biochemical Parameters ◽

Hematological Parameters ◽

Protective Role ◽

Alpha Tocopherol ◽

Post Mortem ◽

Group B ◽

Vitamin E And C

The present study was undertaken to find out the efficacy of vitamin E and/or vitamin C against mercury (Hg) induced toxicity in mice. Sixty mice were randomly divided into 5 equal groups (n=12). One group of mice (Group A) was kept as control and each of rest four groups (B, C, D and E) were fed with mercuric chloride (HgCl2) in drinking water @ 65 mg/L. In addition to HgCl2 alpha-tocopherol (vitamin E) @ 100 mg/L, ascorbic acid (vitamin C) @ 250 mg/L and combination of vitamin E and vitamin C at same dose were given to the mice of groups C, D and E respectively. All treatments were continued for 28 consecutive days. Four mice of each group were sacrificed on day 1, 14 and 28 and efficacy of vitamin E and vitamin C against Hg induced toxicity were evaluated by observing toxic signs, body weight, hemato-biochemical parameters and postmortem lesions. Mild (++) toxic signs as evident by reduced feed and water intake, salivation, vomiting, excitement, muscle tremor, ataxia, restlessness, incordination and ruffled hair coat were observed from 2nd week (group B) and from 3rd week (group C and D) by intoxication with HgCl2. Significant (P<0.01) reduction of body weight (18.38%) and hematological parameters i.e. TEC (19.88%), TLC (27.89%), Hb content (34.09%) and PCV (9.15%) were observed at day 28 in HgCl2 induced intoxicated mice (group B). At identical period in same group biochemical parameters i.e. AST (46.99%) and ALT (58.72%) increased significantly (p<0.01). Pinpoint hemorrhages throughout the liver and highly (++++) congested kidney was also observed at post mortem (group B). All the parameters i.e. toxic signs, body weight, hemato-biochemical and post mortem lesions were found to be slight (+) or mild (++) and/or improved in rest three groups of mice following treatment with vitamin E, vitamin C and combination of vitamin E and vitamin C. The present study reveals that vitamin E and C have a protective role against Hg poisoning. However, combination of vitamin E and C gave better results.DOI: http://dx.doi.org/10.3329/pa.v19i2.16949 Progress. Agric. 19(2): 93 - 100, 2008

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Vitamin E ameliorates disturbances in testosterone pathway and sperm quality of male rats induced by the glycosides vicine and convicine of Vicia faba

Nutrition & Food Science ◽

10.1108/nfs-02-2021-0053 ◽

2021 ◽

Vol ahead-of-print (ahead-of-print) ◽

Author(s):

Khaled M.M. Koriem ◽

Mahmoud S.S. Arbid

Keyword(s):

Vitamin E ◽

Vicia Faba ◽

Sperm Quality ◽

Treated Group ◽

Male Rats ◽

Control Group ◽

Content Type ◽

Paraffin Oil ◽

Male Genital

Purpose This paper aims to design to evaluate the protective effect of vitamin E to ameliorate the disturbances in testosterone pathway and sperm quality of male rats induced by the glycosides vicine (V) and convicine (C) of Vicia faba. Design/methodology/approach Forty male albino rats were divided into five equal groups; control, paraffin oil, V (400 mg/kg) C (150 mg/kg)-treated group, vitamin E (100 mg/kg) + VC-treated group, and vitamin E (200 mg/kg) + VC-treated groups which injected intraperioneally (IP) with 0.5-ml saline, 0.5-ml paraffin oil,V (400 mg/kg) and C (150 mg/kg) of Vicia faba, vitamin E (100 mg/kg) + VC-treated groups, and Vitamin E(200 mg/kg) + VC-treated groups, respectively. Blood and testicular tissue were obtained after one month of the study. The male genital organs were calculated. Testosterone (Ts), luteinizing hormone (LH), follicle stimulating hormone (FSH), dehydroepiandrosterone sulfate (DHEA-SO4), sex hormone binding globulin (SHBG),?-glutamyl transpeptidase (?-GT), glucose-6-phosphate dehydrogenase (G6PD), 3ß-hydroxysteroid dehydrogenase (3ßHSD), lactate dehydrogenase (LDH), spermatozoa concentration, percent of mortality and abnormal sperms were evaluated. Findings The VC-treated group showed significant decrease (p < 0.01) in Ts, DHEA-SO4, G6PD, spermatozoa number and mortality percent, as well as, the male genital organs (testes, epidydemis, seminal vesicle, prostate and vasa deferentia) while significant increase (p < 0.01) was found in LH, FSH, SHBG, LDH, ?-GT, sperms monoclonal Ki-67, and abnormal spermatocytes levels compared with control group. Vitamin E co-injection with VC-treated group returned all these parameters to the normal values. The higher dose of vitamin E (200 mg/kg) was more effect than the lower dose (100 mg/kg). Originality/value Vicia faba contains V and C glycosides. The V and C glycosides in Vicia faba are hydrolyzed by intestinal microflora to aglycones divicine and isouramil, respectively. Divicine and isouramil are highly reactive compounds generating free radicals where divicine and isouramil are the main factors of favism. The V and C glycosides induced disturbances in testosterone pathway and sperm quality of male rats and vitamin E ameliorates these disturbances.

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Short term chronic toxicity of tributyltin on the testes of adult albino rats and the possible protective role of omega-3

Human & Experimental Toxicology ◽

10.1177/0960327120947451 ◽

2020 ◽

pp. 096032712094745

Author(s):

Marwa G Ahmed ◽

Mona El-Demerdash Ibrahim ◽

Hoda R El Sayed ◽

Samah M Ahmed

Keyword(s):

Treated Group ◽

Toxic Effects ◽

Cellular Damage ◽

Antioxidant Defenses ◽

Control Group ◽

Albino Rats ◽

Omega 3 ◽

Group I

The declining rate of male fertility is a growing concern. Tributyltin (TBT) is a well-known endocrine disruptor (ED), that induces imposex in female gastropods and is widely used in various industrial applications. The aim of this study was to evaluate the toxic effects of TBT on the testes of adult albino rats and the possible role of omega-3. Forty two adult male albino rats were divided into five groups; control group (Group I) and four experimental groups: omega-3 treated group, TBT treated group, TBT & omega-3 treated group and follow up group. At the end of the study, the rats were subjected to biochemical, histological, immunohistochemical staining for Ki-67 and seminal examinations. Our results clarfied that TBT induced a significant decrease in testosterone, FSH, LH and serum glutathione peroxidase levels and a significant increase in the serum Malondialdehyde as compared to the control group. Tributyltin induced disorganization and shrinkage of seminiferous tubules, apoptosis, cellular damage and marked reduction in the germinal epithelium. A significant decrease in the cell proliferation and arrested spermatogenesis were also detected. Seminal analysis of TBT group showed a significant affection of all parameters as compared to other groups. Omega-3 ameliorated all of these hazardous effects. Follow up group still showed toxic effects. In conclusion, TBT has a toxic effect on the testis. Increased testicular oxidative stress, cellular damage and arrest of spermatogenesis with attenuation in antioxidant defenses are all contributing factors. Omega-3 can protect against TBT induced reproductive toxicity.

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Serum Metabolomic Response to Low and High Dose Vitamin E Supplementation in Two Randomized Controlled Trials

Current Developments in Nutrition ◽

10.1093/cdn/nzaa067_037 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 1810-1810

Author(s):

Jiaqi Huang ◽

Stephanie Weinstein ◽

Wendy Mack ◽

Howard Hodis ◽

Demetrius Albanes

Keyword(s):

Prostate Cancer ◽

Vitamin E ◽

Cancer Prevention ◽

Low Dose ◽

Alpha Tocopherol ◽

P Value ◽

High Dose ◽

Atbc Study ◽

High Dose Vitamin ◽

Vitamin E Supplementation

Abstract Objectives Vitamin E is an essential micronutrient and critical human antioxidant that has been tested for cancer and cardiovascular preventative effects for decades with conflicting results. For example, prostate cancer incidence was reduced by a low-dose vitamin E supplement in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, but the findings were not replicated by high-dose vitamin E trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT). The present investigation examined the serum metabolomic responses to low- and high-dose vitamin E supplementation in order to gain biological insight into the divergent trial outcomes. Methods We examined baseline and on-study serum samples for 154 men randomly assigned to receive 400 IU vitamin E (as alpha-tocopheryl acetate; ATA) or placebo daily in the Vitamin E Atherosclerosis Prevention Study (VEAPS), and 100 men administered 50 IU ATA or placebo daily in the ATBC Study. Over 970 known metabolites were identified using an ultrahigh-performance LC-MS/MS platform. Linear regression models estimated the change in serum metabolites of men supplemented with vitamin E to those assigned to placebo in VEAPS compared with ATBC. Results Serum alpha-carboxyethyl hydrochroman (CEHC) sulfate, alpha-tocopherol, and beta-/gamma-tocopherol were significantly altered by supplementation with ATA in both the VEAPS and ATBC trials (all P-values ≤ 5.1 × 10−5, the Bonferroni multiple-comparisons corrected statistical threshold). Serum C22 lactone sulfate was also significantly decreased in response to the high-dose vitamin E supplement in VEAPS (β = −0.70, P-value = 8.1 × 10−6), but not altered in the low-dose ATBC trial (β = −0.17, P-value = 0.4). Additionally, changes in several androgenic steroid metabolites were strongly related to the vitamin E supplement-associated change in C22 lactone sulfate only in the high-dose VEAPS trial. Conclusions We found evidence of a dose-dependent vitamin E supplementation effect on a novel C22 lactone sulfate compound as well as several androgenic steroids that may have relevance to previous controlled trial findings for prostate cancer. Funding Sources This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health, U.S. Public Health Service, Department of Health and Human Services.

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Vitamin E Protection of the Liver from Paracetamol in the Rat

Clinical Science ◽

10.1042/cs0470449 ◽

1974 ◽

Vol 47 (5) ◽

pp. 449-459 ◽

Cited By ~ 2

Author(s):

B. E. Walker ◽

J. Kelleher ◽

M. F. Dixon ◽

M. S. Losowsky

Keyword(s):

Vitamin E ◽

Enzyme Activities ◽

Weight Control ◽

Treated Group ◽

Hepatic Necrosis ◽

Control Group ◽

Serum Enzyme ◽

Vitamin E Deficiency ◽

Body Weight Control ◽

Very High

1. Control, vitamin E-deficient, vitamin E-supplemented (deficient with added ‘normal’ intake) and vitamin E-treated rats were given paracetamol at a dose of 25.5 mmol (4 g)/kg body weight. Control rats were also given paracetamol with or without simultaneous vitamin E. 2. Plasma aspartate aminotransferase and alanine aminotransferase activities increased to very high values (mean 2842 and 1241 i.u./l respectively) in the control group, and even higher (mean 8220 and 2320 i.u./l respectively) in the vitamin E-deficient group. 3. In the vitamin E-supplemented group the rises in activity were similar but rather less than in the control group (mean 2417 and 815 i.u./l) and in the vitamin E-treated group only very small rises (mean 177 and 98 i.u./l) were seen. 4. Histological evidence of hepatic necrosis correlated closely with plasma enzyme activities. 5. It appears that paracetamol-induced hepatic necrosis is potentiated in vitamin E deficiency and reduced by prior treatment with α-tocopherol. 6. Vitamin E administered simultaneously with paracetamol at 12.8 or 19.2 mmol/kg also greatly reduced the expected rise in serum enzyme activities. 7. These observations may shed some light on the mechanism of paracetamol-induced hepatic necrosis, and may form a basis for preventing or reducing this lesion in man.

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