Impact of L-Carnitine and Selenium Treatment on Testicular Apoptosis in Rats Exposed to 2.45 GHz Microwave Energy

Saygın, Mustafa; Çalışkan, Sadettin; Ozguner, MF; Gümral, Nurhan; Çömlekçi, Selçuk; Karahan, Nermin

doi:10.7727/wimj.2014.205

Cited by 8 publications

(7 citation statements)

References 43 publications

(39 reference statements)

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“…The changes in these parameter levels support some previous observations of the impact of cellular phone radiation on the testicles. Our findings are in accordance with the findings of many different studies [28,35]. The significant increases in the lipid peroxidation indicator MDA and oxidative DNA damage bio-marker 8-OHdG in the testicles tissue in this study may be due to ROS generated from RFR emitted from cellular phones.…”

Section: Analysis Of Tas Tos Osi 8-ohdg and Mdasupporting

confidence: 93%

“…Another study reported that electromagnetic radiation emitted from Wi-Fi (2450 MHz) and cellular phones (900 and 1800 MHz) causes an increase in lipid peroxidation and a decrease in the levels of antioxidant trace elements (copper and zinc) along with TAS and glutathione (GSH) in the kidneys and testicles of rats in their development periods, and thus leads to oxidative stress [29]. Saygın et al [35] also reported that exposure to electromagnetic radiation emitted by wireless devices (2.45 GHz; 3 h/day, 130 days) led to an increase in the MDA content and TOS value of Sprague-Dawley rats in addition to a decrease in the TAS value. Rago et al [36] reported a statistically significant relationship between the SAR and oxidative DNA damage biomarker 8-OHdG and DNA fragmentation, after exposure to RF-EMR.…”

Section: Analysis Of Tas Tos Osi 8-ohdg and Mdamentioning

confidence: 99%

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Single-strand DNA breaks and oxidative changes in rat testes exposed to radiofrequency radiation emitted from cellular phones

Alkış

Akdağ

Daşdağ

et al. 2019

Biotechnology & Biotechnological Equipment

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The testes are a sensitive organ to electromagnetic pollution and people are concerned about the harmful effects of the radiofrequency radiation (RFR) emitted from cellular phones. Therefore, the purpose of this study was to investigate the effects of long-term exposure to different RFR frequencies on single-strand DNA breaks and oxidative changes in rat testicular tissue. Twenty-eight male Sprague-Dawley rats were divided randomly into four groups. Three groups were exposed to radiation emitted from 900, 1800 and 2100 MHz RF generators, 2 h/day for 6 months. The sham-control group was kept under the same experimental conditions but the RFR generator was turned off. Immediately after the last exposure, testes were removed and DNA damage, 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) were analyzed. The results of this study indicated that RFR increased TOS, OSI, MDA and 8-OHdG (p < 0.05). TAS levels in the exposed group were lower than in the sham group (p < 0.05). In terms of DNA damage, the tail intensities in the comet assay were higher in the exposure groups (p < 0.05). This study demonstrated that long-term exposure to RFR emitted by cellular phones may cause oxidative stress and oxidative DNA damage in rat testicular tissue and may generate DNA single-strand breaks at high frequencies (1800 and 2100 MHz). Our results showed that some RFR emitted from cellular phones has potential to lead to cell damage in the testes.

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Section: Analysis Of Tas Tos Osi 8-ohdg and Mdasupporting

confidence: 93%

Section: Analysis Of Tas Tos Osi 8-ohdg and Mdamentioning

confidence: 99%

Single-strand DNA breaks and oxidative changes in rat testes exposed to radiofrequency radiation emitted from cellular phones

Alkış

Akdağ

Daşdağ

et al. 2019

Biotechnology & Biotechnological Equipment

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“…Our results were in accordance with, 24 who reported that CPX causing decrease in sperm counts and motility in laboratory animals. On the other hand The obtained data are parallel with 25,26 who reported that LC and Co-Q10 attenuated spermatogenic and testicular damage by returning sperm count, motility and viability towards normal control values. A series of enzymatic reactions are required to synthesize testosterone and estrogen from cholesterol.…”

Section: Discussionsupporting

confidence: 80%

L-Carnitine and Co-Enzyme Q10 Ameliorate Ciprofloxacin-Induced Reproductive Toxicity in Male Rats: Regulation of Inflammation and Expression of Steroidogenic Genes

Ali¹,

Atia²,

Rashed³

et al. 2019

Int Res J Pharm

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This study was conducted to evaluate Ciprofloxacin (CPX) reproductive toxicity in 30 days and the protective effect of L-Carnitine (LC) and /or Co-Enzyme Q10 (Co-Q10) against reproductive toxicity induced by CPX and the molecular changes that related to their effects. Animals were divided into 5 groups (12 rats/group). Group 1, was kept as a control. Group 2, was administered CPX (90 mg/kg/day, p.o) and kept as a positive control. Group 3, was co-administered CPX with LC (94.5 mg/kg/day p.o). Group 4, was co-administered CPX with Co-Q10 (8.1 mg/kg/day p.o). Group 5, was concurrently administered CPX with Co-Q10 + LC orally for 30 days. After thirty days, body and genital sex organ weights (testes, prostate glands, and seminal vesicles) and semen analysis (sperm count, motility and morphology), were assayed. Gene expression of StAR, SR-B1, and 3βHSD were assayed by using real-time PCR. Hormonal assay (Testosterone, LH, and FSH), biomarkers of inflammatory mediators (TNF-α) and anti-inflammatory mediators (IL-10) were assayed by using ELISA. MDA, GSH, and TAC were investigated by a spectrophotometer. Results: The thirty-day administration of CPX to adult male rats promotes reproductive toxicity in rats by generating oxidative damage. It induces an adverse effect on reproductive organs weights, sperm parameters, reduction of gene coordination (StAR, SR-B1, and 3 βHSD) and reproductive hormones. Also, increases TNF-α and decreases IL-10 Notably, LC and Co-Q10 co-administration overcame all of these side effects. Conclusion: concurrent administration of both LC and Co-Q10 with CPX ameliorating reproductive toxicity induced by CPX in thirty days administration.

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“…Many studies have demonstrated that Se can protect against hepatocellular oxidative damage induced by lipopolysaccharides [47], renal damage caused by some metallic elements [48], and Aflatoxin B1 [49]. Previous studies also have demonstrated that Se appears to be mediated through its anti-apoptosis and anti-oxidative effects to protect against testis damage caused by ischaemia-reperfusion [23], cisplatin [50], electromagnetic radiation [51], and carbimazole [52]. Our results demonstrated that Se could inhibit testis tissue cells apoptosis caused by ZEN.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effect of Selenium on Chronic Zearalenone-Induced Reproductive System Damage in Male Mice

et al. 2016

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This study aims to explore the protective effect of selenium (Se) on chronic zearalenone (ZEN)-induced reproductive system damage in male mice and the possible protective molecular mechanism against this. The chronic ZEN-induced injury mouse model was established with the continuous intragastric administration of 40 mg/kg body mass (B.M.) ZEN for 28 days. Then, interventions with different doses (0.1, 0.2, and 0.4 mg/kg B.M.) of Se were conducted on mice to analyse the changes in organ indexes of epididymis and testis, antioxidant capability of testis, serum level of testosterone, sperm concentration and motility parameters, and the expression levels of apoptosis-associated genes and blood testis barrier-(BTB) related genes. Our results showed that Se could greatly improve the ZEN-induced decrease of epididymis indexes and testis indexes. Results also showed that the decrease in sperm concentration, sperm normality rate, and sperm motility parameters, including percentage of motile sperm (motile), tropism percentage (progressive) and sperm average path velocity (VAP), caused by ZEN were elevated upon administration of the higher dose (0.4 mg/kg) and intermediate dose (0.2 mg/kg) of Se. Selenium also significantly reduced the content of malondialdehyde (MDA) but enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the testis tissue. Further research demonstrated that ZEN increased the level of mRNA expression of BCL2-associated X protein (Bax) and caspase 3 (Casp3), decreased the level of mRNA expression of B cell leukemia/lymphoma 2 (Bcl2), vimentin (Vim) and cadherin 2 (Cdh2), whereas the co-administration of Se reversed these gene expression levels. Our results indicated that high levels of Se could protect against reproductive system damage in male mice caused by ZEN and the mechanism might such be that Se improved mice antioxidant ability, inhibited reproductive cell apoptosis, and increased the decrease of BTB integrity-related genes caused by ZEN.

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Impact of L-Carnitine and Selenium Treatment on Testicular Apoptosis in Rats Exposed to 2.45 GHz Microwave Energy

Cited by 8 publications

References 43 publications

Single-strand DNA breaks and oxidative changes in rat testes exposed to radiofrequency radiation emitted from cellular phones

Single-strand DNA breaks and oxidative changes in rat testes exposed to radiofrequency radiation emitted from cellular phones

L-Carnitine and Co-Enzyme Q10 Ameliorate Ciprofloxacin-Induced Reproductive Toxicity in Male Rats: Regulation of Inflammation and Expression of Steroidogenic Genes

The Protective Effect of Selenium on Chronic Zearalenone-Induced Reproductive System Damage in Male Mice

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