Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Jun 2:2020:4981386.
doi: 10.1155/2020/4981386. eCollection 2020.

Impact of Coenzyme Q10 Administration on Lead Acetate-Induced Testicular Damage in Rats

Manal El-Khadragy  1   2 , Wafa A Al-Megrin  1 , Norah A AlSadhan  3 , Dina M Metwally  4   5 , Rehab E El-Hennamy  2 , Fatma Elzahraa H Salem  2   6 , Rami B Kassab  2   7 , Ahmed E Abdel Moneim  2
Affiliations

Impact of Coenzyme Q10 Administration on Lead Acetate-Induced Testicular Damage in Rats

Manal El-Khadragy et al. Oxid Med Cell Longev. .

Abstract

Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups (n = 7) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 (v : v), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the concentration of Pb in the testis of rats treated with lead acetate (PbAc, 20 mg/kg). Data was represented as mean ± SEM (n = 7). A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 2
Figure 2
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the absolute and relative testicular weight in rats treated with lead acetate (PbAc, 20 mg/kg). All data represented as mean ± SEM (n = 7). A,BSignificant change at p < 0.05; ∗Significant variation at p < 0.01 as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 3
Figure 3
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the plasma levels of testosterone, LH, and FSH in rats treated with lead acetate (PbAc, 20 mg/kg). All data represented as mean ± SEM (n = 7). A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 4
Figure 4
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on lipid peroxidation (LPO), nitric oxide (NO), and reduced glutathione (GSH) concentrations in the testis of rats treated with lead acetate (PbAc, 20 mg/kg). Data was represented as mean ± SEM (n = 7). A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 5
Figure 5
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and their corresponding mRNA expressions in the testis of rats exposed to lead acetate (PbAc, 20 mg/kg). Data of the antioxidant enzyme activity was represented as mean ± SEM (n = 7), while the values of mRNA expressions (mean ± SEM of triplicate assays) were normalized to the Actb mRNA levels and are expressed as the fold change relative to the control group. A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 6
Figure 6
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the mRNA levels of Nfe212 and Hmox1 in the testes of rats exposed to lead acetate (PbAc, 20 mg/kg). Data was represented as mean ± SEM of triplicate assays. Data was first normalized to the Actb mRNA levels then was expressed as a fold change relative to the control group. A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively.
Figure 7
Figure 7
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the testis of rats treated with lead acetate (PbAc, 20 mg/kg). Data was represented as mean ± SEM (n = 7). A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively.
Figure 8
Figure 8
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the mRNA expression of Bcl2, Bax, and Casp3 in the testes of rats exposed to lead acetate (PbAc, 20 mg/kg). Data was represented as mean ± SEM of triplicate assays. Data was first normalized to the Actb mRNA levels then was expressed as the fold change relative to the control group. A,BSignificant change at p < 0.05; ∗,∗∗Significant variation at p < 0.01 and p < 0.001, respectively, as compared to the control and PbAc groups, respectively. Data was analyzed by one-way ANOVA using Duncan's post hoc test.
Figure 9
Figure 9
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the caspase-3 expression in the testis tissue after lead acetate (PbAc, 20 mg/kg) exposure. (a) Control group, (b) CoQ10-administered group, (c) PbAc-exposed group, and (d) PbAc+CoQ10-treated group. Scale bar = 100 μm.
Figure 10
Figure 10
Effects of coenzyme Q10 (CoQ10, 10 mg/kg) administration on the histopathological changes in the testis tissue after lead acetate (PbAc, 20 mg/kg) exposure. (a) Control group, (b) CoQ10-administered group, (c) PbAc-exposed group, and (d) PbAc+CoQ10-treated group. Scale bar = 100 μm.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Kumar S. R., Devi A. S. Lead toxicity on male reproductive system and its mechanism: a review. Research Journal of Pharmacy and Technology. 2018;11(3):p. 1228. doi: 10.5958/0974-360x.2018.00228.7. - DOI
    1. Rossi-George A., Virgolini M. B., Weston D., Thiruchelvam M., Cory-Slechta D. A. Interactions of lifetime lead exposure and stress: behavioral, neurochemical and HPA axis effects. Neurotoxicology. 2011;32(1):83–99. doi: 10.1016/j.neuro.2010.09.004. - DOI - PMC - PubMed
    1. Zuscik M. J., Ma L., Buckley T., et al. Lead induces chondrogenesis and alters transforming growth factor-beta and bone morphogenetic protein signaling in mesenchymal cell populations. Environmental Health Perspectives. 2007;115(9):1276–1282. doi: 10.1289/ehp.10028. - DOI - PMC - PubMed
    1. Nash D., Magder L., Lustberg M., et al. Blood lead, blood pressure, and hypertension in perimenopausal and postmenopausal women. JAMA. 2003;289(12):1523–1532. doi: 10.1001/jama.289.12.1523. - DOI - PubMed
    1. Hassan E., El-Neweshy M., Hassan M., Noreldin A. Thymoquinone attenuates testicular and spermotoxicity following subchronic lead exposure in male rats: possible mechanisms are involved. Life Sciences. 2019;230:132–140. doi: 10.1016/j.lfs.2019.05.067. - DOI - PubMed

MeSH terms