The Effect of Diazinon on Cell Proliferation and Apoptosis in Testicular Tissue of Rats and The Protective Effect of Vitamin E

Rahimi Anbarkeh F, Nikravesh MR, Jalali M, Sadeghnia HR, Sargazi Z

Int J Fertil Steril. 2019 Jul;13(2):154-160. doi: 10.22074/ijfs.2019.5612. Epub 2019 Apr 27.

Abstract

BACKGROUND:

Diazinon (DZN) is an organophosphate pesticide, and nowadays this pesticide is mostly used in agriculture. In this study, we analyzed the effects of DZN and vitamin E (Vit E) on apoptosis and the proliferation of germ cells in rat testis.

MATERIALS AND METHODS:

In this experimental study, 30 male Wistar rats were divided into five groups (n=6 per group) consisting of control, sham (received olive oil), experimental group i (60 mg/kg DZN), experimental group ii (60 mg/kg DZN and 200 mg/kg Vit E), and experimental group iii (200 mg/kg Vit E). After six weeks, left testis of rats was removed for the detection of proliferative cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase end-labeling (TUNEL).

RESULTS:

Compared with the control group, DZN in the experimental group i decreased the number of PCNA-positive cells and increased the number of TUNEL-positive cells (P<0.001). Vit E improved detrimental changes by the decrease in the rate of apoptosis and the increase in the proliferation of testicular germ cells (P<0.001).

CONCLUSION:

Vit E can decrease the number of TUNEL-positive cells and increase the number of PCNA-positive cells by the neutralization of the toxicity caused by DZN in the testicular tissue.

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Antioxidant supplementation during illness in dogs: effect on oxidative stress and outcome, a pilot study

Hagen DM, Ekena JL, Geesaman BM, Viviano KR

J Small Anim Pract. 2019 Jul 10. doi: 10.1111/jsap.13050. [Epub ahead of print]

Abstract

OBJECTIVES:

To assess whether combination antioxidant supplementation for 30 days in systemically ill dogs alters antioxidant status, degree of lipid peroxidation, clinical score and survival.

MATERIALS AND METHODS:

Forty client-owned systemically-ill hospitalised dogs were eligible for inclusion. Dogs were randomised to no supplementation (NS; n=19) or supplementation with N-acetylcysteine/S-adenosylmethionine/silybin and vitamin E (AS; n=20) for 30 days. Clinical score and oxidative biomarkers including glutathione, cysteine, vitamin E, selenium and urine isoprostanes/creatinine (F2 -IsoPs/Cr) were determined on days 0 and 30. Glutathione, cysteine, vitamin E and urine F2 -IsoPs/Cr were quantified by high-performance liquid chromatography, and selenium concentrations determined using atomic absorption spectroscopy.

RESULTS:

Thirty-two dogs completed the study (NS, n=16; AS, n=16). Vitamin E concentrations were significantly greater in the supplemented compared to the non-supplemented group. No other markers of oxidative stress significantly changed with supplementation. There was no difference in Day 30 clinical scores or survival between the two groups.

CLINICAL SIGNIFICANCE:

In this population of systemically-ill hospitalised dogs, combination antioxidant supplementation did not alter redox state or clinical outcome.

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Familial vitamin E deficiency: Multiorgan complications support the adverse role of oxidative stress

Trotta E, Bortolotti S, Fugazzotto G, Gellera C, Montagnese S, Amodio P

Nutrition. 2019 Jul - Aug;63-64:57-60. doi: 10.1016/j.nut.2018.11.012. Epub 2018 Dec 1.

Abstract

Vitamin E is an essential micronutrient with relevant antioxidant and anti-inflammatory properties found in plant leaves, seeds, and products derived from their processing. Familial vitamin E deficiency is a rare inherited syndrome characterized by ataxia and peripheral neuropathy with a massive decrease in plasma vitamin E (<0.5 mg/dL). This report describes the history of two siblings suffering from ataxia with vitamin E deficiency who developed premature systemic disorders (atherosclerotic vascular disease, ischemic heart disease, and liver steatosis) in absence of relevant risk factors. The association of neuromuscular symptoms and multiorgan involvement in patients with ataxia with vitamin E deficiency has not been reported to our knowledge. The lack of an effective vitamin E activity seems to be implicated in the pathogenesis of cardiovascular, gastrointestinal, and other diseases in which oxidative stress is a risk factor.

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Beneficial effects of vitamin E on radioiodine induced gastrointestinal damage: an experimental and pathomorphological study.

Yumusak N, Sadic M, Akbulut A, Aydinbelge FN, Koca G, Korkmaz M

Bratisl Lek Listy. 2019;120(4):263-269. doi: 10.4149/BLL_2019_048.

Abstract

OBJECTIVES:

The aim of the present study was to investigate the radioprotective effect of vitamin E in the prevention of radioiodine (RAI) induced gastrointestinal damage.

METHOD:

Twenty-four rats were randomly divided into three groups as follows: Group-1 was untreated control group, Group-2 was orally administered single dose of 111 MBq RAI, and Group-3 was orally administered 111 MBq RAI and 1 mL of oral vitamin EVitamin E was started two days before RAI administration and was continued for five days once daily after RAI. Pathomorphological parameters of gastrointestinal tissues (stomach, small intestines and bowels) were measured using Hematoxylin-Eosin and Masson’s trichrome staining.

RESULTS:

Varying degrees of inflammation, edema, ulcer, mucosal degeneration, necrosis and fibrosis were seen in the stomach, small intestine and bowel tissues of the rats in both study groups and not in the control group. The differences were statistically significant between these groups for all parameters (p < 0.05). The histopathological damage in the vitamin E treated group was significantly less than the damage in the RAI only group (p < 0.05 for all pathomorphological parameters).

CONCLUSION:

The results of this study showed that vitamin E has a radioprotective property with antiinflammatory and antifibrotic effects protecting against gastrointestinal damage caused by radioiodine.

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Familial vitamin E deficiency: Multiorgan complications support the adverse role of oxidative stress

Trotta E, Bortolotti S, Fugazzotto G, Gellera C, Montagnese S, Amodio P

Nutrition. 2019 Jul - Aug;63-64:57-60. doi: 10.1016/j.nut.2018.11.012. Epub 2018 Dec 1.

Abstract

Vitamin E is an essential micronutrient with relevant antioxidant and anti-inflammatory properties found in plant leaves, seeds, and products derived from their processing. Familial vitamin E deficiency is a rare inherited syndrome characterized by ataxia and peripheral neuropathy with a massive decrease in plasma vitamin E (<0.5 mg/dL). This report describes the history of two siblings suffering from ataxia with vitamin E deficiency who developed premature systemic disorders (atherosclerotic vascular disease, ischemic heart disease, and liver steatosis) in absence of relevant risk factors. The association of neuromuscular symptoms and multiorgan involvement in patients with ataxia with vitamin E deficiency has not been reported to our knowledge. The lack of an effective vitamin E activity seems to be implicated in the pathogenesis of cardiovascular, gastrointestinal, and other diseases in which oxidative stress is a risk factor.

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Vitamin E – An Antioxidant & Immunity Fat Soluble Vitamin

Vitamin E is an antioxidant. Antioxidants are substances that may protect your cells against the effects of free radicals. Free radicals are molecules produced when your body breaks down food, or by environmental exposures like tobacco smoke and radiation. Vitamin E also plays a role in your immune system and metabolic processes. Good sources of vitamin E are vegetable oils, margarine, nuts, seeds, and some leafy greens, but not all. Vitamin E is also added to foods like cereals. Most people get enough vitamin E from the foods they eat. People with certain disorders, such as liver diseases, cystic fibrosis, and Crohn’s disease may need extra vitamin E.

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Vitamin E δ-tocotrienol sensitizes human pancreatic cancer cells to TRAIL-induced apoptosis through proteasome-mediated down-regulation of c-FLIPs

Francois RA, Zhang A, Husain K, Wang C, Hutchinson S, Kongnyuy M, Batra SK, Coppola D, Sebti SM, Malafa MP

Cancer Cell Int. 2019 Jul 22;19:189. doi: 10.1186/s12935-019-0876-0. eCollection 2019.

Abstract

BACKGROUND:

Vitamin E δ-tocotrienol (VEDT), a vitamin E compound isolated from sources such as palm fruit and annatto beans, has been reported to have cancer chemopreventive and therapeutic effects.

METHODS:

We report a novel function of VEDT in augmenting tumor necrosis factor-related apoptosis-inducing ligand- (TRAIL-) induced apoptosis in pancreatic cancer cells. The effects of VEDT were shown by its ability to trigger caspase-8-dependent apoptosis in pancreatic cancer cells.

RESULTS:

When combined with TRAIL, VEDT significantly augmented TRAIL-induced apoptosis of pancreatic cancer cells. VEDT decreased cellular FLICE inhibitory protein (c-FLIP) levels without consistently modulating the expression of decoy death receptors 1, 2, 3 or death receptors 4 and 5. Enforced expression of c-FLIP substantially attenuated VEDT/TRAIL-induced apoptosis. Thus, c-FLIP reduction plays an important part in mediating VEDT/TRAIL-induced apoptosis. Moreover, VEDT increased c-FLIP ubiquitination and degradation but did not affect its transcription, suggesting that VEDT decreases c-FLIP levels through promoting its degradation. Of note, degradation of c-FLIP and enhanced TRAIL-induced apoptosis in pancreatic cancer cells were observed only with the anticancer bioactive vitamin E compounds δ-, γ-, and β-tocotrienol but not with the anticancer inactive vitamin E compounds α-tocotrienol and α-, β-, γ-, and δ-tocopherol.

CONCLUSIONS:

c-FLIP degradation is a key event for death receptor-induced apoptosis by anticancer bioactive vitamin E compounds in pancreatic cancer cells. Moreover, VEDT augmented TRAIL inhibition of pancreatic tumor growth and induction of apoptosis in vivo. Combination therapy with TRAIL agonists and bioactive vitamin E compounds may offer a novel strategy for pancreatic cancer intervention.

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The Effect of Alpha-Tocopherol on Morphine Tolerance-induced Expression of c-fos Proto-oncogene from a Biotechnological Perspective

Mehrabi S, Nasirinezhad F, Barati M, Abutaleb N, Barati S, Dereshky BT, Amini N, Milan PB, Jahanmahin A, Sarveazad A, Samadikuchaksaraei A, Mozafari M

Recent Pat Biotechnol. 2019;13(2):137-148. doi: 10.2174/1872208312666181120105333.

Abstract

BACKGROUND:

The increase of oxidant compounds is the most well-known reasons for the tolerance to the analgesic properties of Morphine. Additionally, the production of proxy-nitrite impairs receptors, proteins and enzymes involved in the signaling pathways of analgesia, apoptosis and necrosis. Also, we revised all patents relating to opioid tolerance control methods.

OBJECTIVE:

The aim of this study was to assess the effects of Alpha-tocopherol as an anti-oxidant agent to reduce Morphine tolerance.

METHOD:

Forty male rats randomly divided into four groups. 10 mg/kg of morphine was injected subcutaneously to create the desired level of tolerance. After modeling, 70 mg/kg Alpha- Tocopherol was injected intraperitoneal. Also, the hot plate recorded pain threshold alterations was used to evaluate the behavioral test. All tissue samples were extracted from the spinal cord, thalamus and frontal cortex for molecular and gene expression evaluations. Also, the effect of Alpha- Tocopherol on the apoptosis and necrosis parameters was analyzed using nissl staining and tunel test.

RESULTS:

The time latency results showed that there were no significant differences in the different days in groups treated with Morphine plus Alpha-Tocopherol. However, our data highlighted that the pain threshold and their time latency in respond to it had substantially increased in comparison with the control group. Furthermore, we found that the Alpha-Tocopherol obviously decreased c-fos gene expression, especially in the spinal cord.

CONCLUSION:

Thus, co-administration of Alpha-Tocopherol with Morphine can decrease the adverse effects of nitrite proxy, which is released due to repeated injections of Morphine.

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Alpha-tocopherol in intravenous lipid emulsions imparts hepatic protection in a murine model of hepatosteatosis induced by the enteral administration of a parenteral nutrition solution

Fell GL, Anez-Bustillos L, Dao DT, Baker MA, Nandivada P, Cho BS, Pan A, O'Loughlin AA, Nose V, Gura KM, Puder M

PLoS One. 2019 Jul 11;14(7):e0217155. doi: 10.1371/journal.pone.0217155. eCollection 2019.

Abstract

Intestinal failure-associated liver disease (IFALD) is a risk of parenteral nutrition (PN)-dependence. Intravenous soybean oil-based parenteral fat can exacerbate the risk of IFALD while intravenous fish oil can minimize its progression, yet the mechanisms by which soybean oil harms and fish oil protects the liver are uncertain. Properties that differentiate soybean and fish oils include α-tocopherol and phytosterol content. Soybean oil is rich in phytosterols and contains little α-tocopherol. Fish oil contains abundant α-tocopherol and little phytosterols. This study tested whether α-tocopherol confers hepatoprotective properties while phytosterols confer hepatotoxicity to intravenous fat emulsions. Utilizing emulsions formulated in the laboratory, a soybean oil emulsion (SO) failed to protect from hepatosteatosis in mice administered a PN solution enterally. An emulsion of soybean oil containing α-tocopherol (SO+AT) preserved normal hepatic architecture. A fish oil emulsion (FO) and an emulsion of fish oil containing phytosterols (FO+P) protected from steatosis in this model. Expression of hepatic acetyl CoA carboxylase (ACC) and peroxisome proliferator-activated receptor gamma (PPARγ), was increased in animals administered SO. ACC and PPARγ levels were comparable to chow-fed controls in animals receiving SO+AT, FO, and FO+P. This study suggests a hepatoprotective role for α-tocopherol in liver injury induced by the enteral administration of a parenteral nutrition solution. Phytosterols do not appear to compromise the hepatoprotective effects of fish oil.

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Combination Effect of Bowman-Birk Inhibitor and α-Tocopheryl Succinate on Prostate Cancer Stem-Like Cells

Kaneko S, Yamazaki T, Kohno K, Sato A, Kato K, Yano T

J Nutr Sci Vitaminol (Tokyo). 2019;65(3):272-277. doi: 10.3177/jnsv.65.272.

Abstract

The reoccurrence of androgen-dependent prostate cancer after anti-androgen therapy mainly depends on prostate cancer stem-like cells. To reduce the risk, it is important to delete the cancer stem-like cells. Furthermore, to induce differentiation of cancer stem-like cells is critical to abrogate stemness of the cells. Therefore, we tried to investigate a possibility on the establishment of a new effective therapy to eradicate the cancer stem-like cells via the induction of differentiation in this study. Prostate cancer stem-like cells from an androgen-dependent prostate cancer cell line (LNCaP cell) had severe resistance against an anti-androgen therapeutic agent. We selected Bowman-Birk inhibitor (BBI) from soybeans reported as a chemopreventive agent in prostate cancer to differentiate the caner stem-like cells and α-tocopheryl succinate (TOS) known as a mitocan to induce effectively cytotoxic effect against the cancer stem-like cells. In fact, only TOS treatment had cytotoxic effect against the cancer stem-like cells, but the addition of BBI treatment to the cells treated with TOS reinforced TOS-mediated cytotoxicity in the cancer stem-like cells. This reinforcement coincided with the combination-enhanced apoptosis in the stem-like cells. Also, we confirmed caspase9-caspase3 cascade mainly contributed to the enhancement of the cytotoxicity in the stem-like cells caused by the combination, indicating that the reinforcement of BBI on TOS-mediated apoptosis via mitochondria related to the enhancing cytotoxic effect of the combination on the prostate cancer stem-like cells. Overall, it seems that the combination is an effective new approach to reduce the reoccurrence of prostate cancer targeting prostate cancer stem cells.

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