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Molecular basis for the effects of zinc deficiency on spermatogenesis: An experimental study in the Sprague-dawley rat model.

Omu AE, Al-Azemi MK, Al-Maghrebi M, Mathew CT, Omu FE, Kehinde EO, Anim JT, Oriowo MA, Memon A - Indian J Urol (2015 Jan-Mar)

Bottom Line: The objective of this study is to investigate the molecular mechanisms underlying the effects of zinc deficiency on spermatogenesis in the Sprague-Dawley (SD) rat.Zinc deficiency is associated with impaired spermatogenesis because of reduced testosterone production, increased oxidative stress and apoptosis.These findings suggest that zinc has a role in male reproduction.

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynaecology, Faculty of Medicine, Kuwait University, Kuwait.

ABSTRACT

Introduction: The objective of this study is to investigate the molecular mechanisms underlying the effects of zinc deficiency on spermatogenesis in the Sprague-Dawley (SD) rat.

Materials and methods: Three groups of eight adult male SD rats were maintained for 4 weeks on a normal diet as control, zinc deficient diet and zinc deficient diet with zinc supplementation of 28 mg zinc/kg body weight respectively. Using standard techniques, the following parameters were compared between the three groups of experimental animals at the end of 4 weeks: (a) Serum zinc, magnesium (Mg), copper (Cu), selenium (Se) and cadmium (Cd), (b) serum sex hormones, malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX), (c) interleukin-4 (IL-4), tumor necrosis factor-alpha (TNF-α), Bcl-2, Bax and caspase-3 expression in the testes, (d) assessment of apoptosis of testicular cells using electron microscopy and (e) testicular volume and histology using the orchidometer and Johnsen score, respectively.

Results: The zinc deficient group showed a reduction of testicular volume, serum concentrations of Zn, Cu, Se, Mg, SOD, GPX, IL-4, Bcl-2 and testosterone (P < 0.05), as well as increased levels of serum Cd, MDA and tissue TNF-α, Bax, caspase-3 and apoptosis of the germ cells (P < 0.05) compared with control and zinc supplementation groups.

Conclusion: Zinc deficiency is associated with impaired spermatogenesis because of reduced testosterone production, increased oxidative stress and apoptosis. These findings suggest that zinc has a role in male reproduction.

No MeSH data available.


Related in: MedlinePlus

Immunohistochemical staining with Bcl-2, caspase-3 and Bax (×250) of rats fed normal diet (a), zinc deficient diet (b) and zinc supplementation diet (c). These staining reactions show the following: *Intense staining with Bcl-2 of mature spermatozoa *Intense staining with Bax (black) and caspase-3 (red) consistent with increased apoptosis of the early germ cells such as spermatogonia, spermatocytes and spermatids associated with zinc deficiency *intense staining with Bcl-2 of mature spermatozoa in the seminiferous tubule of rats fed with zinc supplementation diet
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Figure 2: Immunohistochemical staining with Bcl-2, caspase-3 and Bax (×250) of rats fed normal diet (a), zinc deficient diet (b) and zinc supplementation diet (c). These staining reactions show the following: *Intense staining with Bcl-2 of mature spermatozoa *Intense staining with Bax (black) and caspase-3 (red) consistent with increased apoptosis of the early germ cells such as spermatogonia, spermatocytes and spermatids associated with zinc deficiency *intense staining with Bcl-2 of mature spermatozoa in the seminiferous tubule of rats fed with zinc supplementation diet

Mentions: Table 4 and Figure 2 show the immunohistochemical staining for Bcl-2, Bax, caspase-3 for the 3 groups of animals. There was increased expression of Bax and caspase-3 in the zinc deficient group of rats compared to control or zinc supplementation group of rats. Caspase-3 activity was reduced by about 50% in the zinc supplementation group compared with control group, while it was increased by about 100% in zinc deficient group compared with control group (P < 0.05). Bcl-2 was highly expressed in the zinc supplementation and the control groups, but least expressed in the zinc deficient group. Figure 2 shows immunohistochemical staining of the testis. Figure 2a shows intense staining with Bcl-2 in mature spermatozoa associated with normal zinc status and with zinc supplementation as shown on Figure 2c, while Figure 2b revealed marked staining with Bax and caspase-3 in association with zinc deficiency.


Molecular basis for the effects of zinc deficiency on spermatogenesis: An experimental study in the Sprague-dawley rat model.

Omu AE, Al-Azemi MK, Al-Maghrebi M, Mathew CT, Omu FE, Kehinde EO, Anim JT, Oriowo MA, Memon A - Indian J Urol (2015 Jan-Mar)

Immunohistochemical staining with Bcl-2, caspase-3 and Bax (×250) of rats fed normal diet (a), zinc deficient diet (b) and zinc supplementation diet (c). These staining reactions show the following: *Intense staining with Bcl-2 of mature spermatozoa *Intense staining with Bax (black) and caspase-3 (red) consistent with increased apoptosis of the early germ cells such as spermatogonia, spermatocytes and spermatids associated with zinc deficiency *intense staining with Bcl-2 of mature spermatozoa in the seminiferous tubule of rats fed with zinc supplementation diet
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4300574&req=5

Figure 2: Immunohistochemical staining with Bcl-2, caspase-3 and Bax (×250) of rats fed normal diet (a), zinc deficient diet (b) and zinc supplementation diet (c). These staining reactions show the following: *Intense staining with Bcl-2 of mature spermatozoa *Intense staining with Bax (black) and caspase-3 (red) consistent with increased apoptosis of the early germ cells such as spermatogonia, spermatocytes and spermatids associated with zinc deficiency *intense staining with Bcl-2 of mature spermatozoa in the seminiferous tubule of rats fed with zinc supplementation diet
Mentions: Table 4 and Figure 2 show the immunohistochemical staining for Bcl-2, Bax, caspase-3 for the 3 groups of animals. There was increased expression of Bax and caspase-3 in the zinc deficient group of rats compared to control or zinc supplementation group of rats. Caspase-3 activity was reduced by about 50% in the zinc supplementation group compared with control group, while it was increased by about 100% in zinc deficient group compared with control group (P < 0.05). Bcl-2 was highly expressed in the zinc supplementation and the control groups, but least expressed in the zinc deficient group. Figure 2 shows immunohistochemical staining of the testis. Figure 2a shows intense staining with Bcl-2 in mature spermatozoa associated with normal zinc status and with zinc supplementation as shown on Figure 2c, while Figure 2b revealed marked staining with Bax and caspase-3 in association with zinc deficiency.

Bottom Line: The objective of this study is to investigate the molecular mechanisms underlying the effects of zinc deficiency on spermatogenesis in the Sprague-Dawley (SD) rat.Zinc deficiency is associated with impaired spermatogenesis because of reduced testosterone production, increased oxidative stress and apoptosis.These findings suggest that zinc has a role in male reproduction.

View Article: PubMed Central - PubMed

Affiliation: Department of Obstetrics and Gynaecology, Faculty of Medicine, Kuwait University, Kuwait.

ABSTRACT

Introduction: The objective of this study is to investigate the molecular mechanisms underlying the effects of zinc deficiency on spermatogenesis in the Sprague-Dawley (SD) rat.

Materials and methods: Three groups of eight adult male SD rats were maintained for 4 weeks on a normal diet as control, zinc deficient diet and zinc deficient diet with zinc supplementation of 28 mg zinc/kg body weight respectively. Using standard techniques, the following parameters were compared between the three groups of experimental animals at the end of 4 weeks: (a) Serum zinc, magnesium (Mg), copper (Cu), selenium (Se) and cadmium (Cd), (b) serum sex hormones, malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GPX), (c) interleukin-4 (IL-4), tumor necrosis factor-alpha (TNF-α), Bcl-2, Bax and caspase-3 expression in the testes, (d) assessment of apoptosis of testicular cells using electron microscopy and (e) testicular volume and histology using the orchidometer and Johnsen score, respectively.

Results: The zinc deficient group showed a reduction of testicular volume, serum concentrations of Zn, Cu, Se, Mg, SOD, GPX, IL-4, Bcl-2 and testosterone (P < 0.05), as well as increased levels of serum Cd, MDA and tissue TNF-α, Bax, caspase-3 and apoptosis of the germ cells (P < 0.05) compared with control and zinc supplementation groups.

Conclusion: Zinc deficiency is associated with impaired spermatogenesis because of reduced testosterone production, increased oxidative stress and apoptosis. These findings suggest that zinc has a role in male reproduction.

No MeSH data available.


Related in: MedlinePlus