**4.7 Assessment of the GPX activity in the testicular and epididymal tissues of male Wistar rats subjected to various treatments**

The results of testicular GPX activity of rats treated with STZ, KV, and/ or IN are captured in **Table 1**. A significantly lower testicular GPx activity was observed in diabetic rats compared to the N group (3.977 ± 0.880 μmol/mg versus 12.26 ± 0.644 μmol/mg, p < 0.05). The nondiabetic rats treated with KV (N + KV) did not show any significant difference in testicular GPx activity compared to the N group. The testes of KV-treated diabetic rats (D + KV) showed significantly higher

**305**

control.

**5. Discussion**

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced…*

**D: diabetic group**

**Group/treatments**

0.193 ± 0.010 0.198 ± 0.008 0.195 ± 0.019 0.169 ± 0.010 0.171 ± 0.020

18.00 ± 0.62\* 12.95 ± 0.58 15.58 ± 1.31\*# 13.60 ± 0.94\$ 11.86 ± 0.54&

12.28 ± 0.227 \*\$& 3.977 ± 0.280 12.06 ± 0.242\*\$ 6.770 ± 0.232 \*#\$& 8.006 ± 0.345\*&

0.055 ± 0.002 \* 0.042 ± 0.002 0.050 ± 0.003 0.052 ± 0.002\* 0.053 ± 0.002\*

2.518 ± 0.178 \*#\$ 4.962 ± 0.807 4.433 ± 0.947\*# 4.896 ± 0.385\* 5.360 ± 0.369&

12.30 ± 0.225\* 4.277 ± 0.279 11.81 ± 0.2476\*\$ 7.056 ± 0.2484\*#\$& 8.006 ± 0.3624\*&

**D + KV: diabetic group treated with Kolaviron**

**D + IN: diabetic group treated with insulin (standard drug)**

**N + KV: nondiabetic group treated with Kolaviron**

GPx activity when compared to the D group. In addition, a significantly higher testicular GPx activity was observed in the D + IN group when compared to the D group. Diabetes induction significantly lowered epididymal GPX activity in comparison to the nondiabetic rats (4.277 ± 0.884 μmol/mg versus 12.30 ± 0.636 μmol/mg, p < 0.05). The supplementation of KV to nondiabetic rats (N + KV) did not significantly alter GPx activity of epididymal tissue compared to the N group. However, epididymal GPX activity was significantly higher in diabetic rats treated with KV compared to the untreated diabetic group Likewise, the treatment of diabetic rats with insulin significantly increased epididymal GPx activity compared to diabetic

*Antioxidant (SOD, CAT, and GPx) activities in testicular and epididymal tissues of Wistar rats after a 6-week* 

*Data are presented as mean ± SEM. N, nondiabetic control group; D, diabetic group; N + KV, nondiabetic group treated with KV; D + KV, diabetic group treated with KV; D + IN, diabetic group treated with insulin (standard* 

Diabetes associated with OS is said to impair testicular and epididymal tissue functions which can generate male infertility [8, 11, 13, 14]. Increasingly, studies demonstrate the significant impact of phytochemicals such as flavonoids in the prevention and treatment of complications related to diabetes [20, 21]. The physiological role and properties of flavonoids in the management of OS are currently being investigated in relation to male infertility. This interest is the motivation for the current study to investigate the effects of KV (KV), a known flavonoid extract of *G. kola,* on testicular- and epididymal-induced OS using a diabetic rat model.

*DOI: http://dx.doi.org/10.5772/intechopen.84822*

**N: nondiabetic control group**

*Represents a significant difference when compared to D*

*Represents significance when compared to D + KV*

*Represents a significant difference when compared to N + KV*

*&Represents a significant difference when compared to D + IN (n = 12 per group)*

**Sample types and tests**

*Testicular* SOD (μmol/mg protein)

CAT (μmol/mg protein)

GPx (μmol/mg protein)

CAT (μmol/mg protein)

GPx (μmol/mg protein)

*drug) \**

**Table 1.**

*period of treatment.*

*#*

*\$*

*Epididymal* SOD (μmol/mg protein)

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced… DOI: http://dx.doi.org/10.5772/intechopen.84822*


*treated with KV; D + KV, diabetic group treated with KV; D + IN, diabetic group treated with insulin (standard drug)*

*\* Represents a significant difference when compared to D*

*# Represents a significant difference when compared to N + KV*

*\$ Represents significance when compared to D + KV*

*&Represents a significant difference when compared to D + IN (n = 12 per group)*

#### **Table 1.**

*Antioxidants*

betic drug.

**subjected to various treatments**

compared to the diabetic control rats.

levels was observed in the testes of KV-treated diabetic rats when compared to the D + IN group (0.007 ± 0.001 μmol/g versus 0.012 ± 0.001 μmol/g, p < 0.05). **Figure 8** shows the MDA level in epididymis of both nondiabetic and diabetic groups treated with KV and/or insulin. The MDA level was significantly higher in epididymal tissue of the D group compared to the N group in epididymal tissue (0.009 ± 0.004 μmol/g versus 0.006 ± 0.002 μmol/g, p < 0.05). No significant differences in MDA levels were observed in the epididymal tissue of nondiabetic rats supplemented with KV (N + KV) compared to the untreated (N) rats. Furthermore, a significantly lower epididymal MDA level was observed in the D + KV group when compared to the D group. KV treatment normalized epididymal MDA level in diabetic rats, and this effect is comparable to that of insulin, the standard antidia-

**4.5 Assessment of SOD activity in testicular and epididymal tissues of rats** 

epididymis are comparable to that of the standard drug, insulin.

**male Wistar rats subjected to various treatments**

**male Wistar rats subjected to various treatments**

As shown in **Table 1**, no significant differences were observed in the activity of testicular superoxide dismutase (SOD) across all treatment groups. However, in the epididymal tissue, the SOD activity was significantly reduced in the diabetic (D) group when compared to the N group (0.042 ± 0.007 μmol/mg, p < 0.05 versus 0.556 ± 0.007 μmol/mg, p < 0.05). On the other hand, separate treatments of diabetic rats with KV and insulin increased SOD activity in epididymal tissue compared to untreated diabetic rats. The effects of KV on the activity of SOD in the

**4.6 Assessment of the catalase activity in testicular and epididymal tissues of** 

A significantly lower CAT activity was observed in testicular tissue of STZ-induced diabetic rats (**Table 1**) in comparison to nondiabetic rats

(12.21 ± 1.235 μmol/mg versus 18.00 ± 1.524 μmol/mg, p < 0.05). The supplementation of KV to nondiabetic rats (N + KV) did not significantly affect testicular CAT activity in comparison to the untreated nondiabetic group. KV treatment of diabetic rats elevated testicular CAT activity in comparison to diabetic control, and CAT activity was restored to normalcy. Likewise, a significantly higher testicular CAT activity was observed after insulin treatment in diabetic rats (D + IN) when

As shown in **Table 1**, STZ-induced diabetic rats showed significantly lower CAT

activity in epididymal tissue compared to the N group (2.864 ± 0.415 μmol/mg versus 6.162 ± 0. 612 μmol/mg, p < 0.05). There was no significant difference in the epididymal CAT activity of rats supplemented with KV (N + KV) when compared to the N group. The separate treatment of diabetic rats with KV and insulin significantly elevated CAT activity in the epididymis compared to the diabetic controls.

**4.7 Assessment of the GPX activity in the testicular and epididymal tissues of** 

The results of testicular GPX activity of rats treated with STZ, KV, and/ or IN are captured in **Table 1**. A significantly lower testicular GPx activity was observed in diabetic rats compared to the N group (3.977 ± 0.880 μmol/mg versus 12.26 ± 0.644 μmol/mg, p < 0.05). The nondiabetic rats treated with KV (N + KV) did not show any significant difference in testicular GPx activity compared to the N group. The testes of KV-treated diabetic rats (D + KV) showed significantly higher

**304**

*Antioxidant (SOD, CAT, and GPx) activities in testicular and epididymal tissues of Wistar rats after a 6-week period of treatment.*

GPx activity when compared to the D group. In addition, a significantly higher testicular GPx activity was observed in the D + IN group when compared to the D group.

Diabetes induction significantly lowered epididymal GPX activity in comparison to the nondiabetic rats (4.277 ± 0.884 μmol/mg versus 12.30 ± 0.636 μmol/mg, p < 0.05). The supplementation of KV to nondiabetic rats (N + KV) did not significantly alter GPx activity of epididymal tissue compared to the N group. However, epididymal GPX activity was significantly higher in diabetic rats treated with KV compared to the untreated diabetic group Likewise, the treatment of diabetic rats with insulin significantly increased epididymal GPx activity compared to diabetic control.

#### **5. Discussion**

Diabetes associated with OS is said to impair testicular and epididymal tissue functions which can generate male infertility [8, 11, 13, 14]. Increasingly, studies demonstrate the significant impact of phytochemicals such as flavonoids in the prevention and treatment of complications related to diabetes [20, 21]. The physiological role and properties of flavonoids in the management of OS are currently being investigated in relation to male infertility. This interest is the motivation for the current study to investigate the effects of KV (KV), a known flavonoid extract of *G. kola,* on testicular- and epididymal-induced OS using a diabetic rat model.

## **5.1 Evaluation of induced diabetes with STZ before KV and insulin treatment**

In the current study, the single intraperitoneal administration of STZ (50 mg/kg) in adult Wistar rats was effective in causing hyperglycemia after 5 days. This was confirmed by the significantly higher plasma glucose levels (18 mmol/l, see **Figure 3**) in the STZ group of animals which is typical of type 1 diabetes mellitus. It was therefore concluded that the diabetic animal model was successfully created and the results were similar to and supported by previous findings [42, 43] where induction of DM in Wistar rats via intravenous STZ injection (of 40 and 45 mg/kg/b.w, respectively) were confirmed by hyperglycemia after 4 days and maintained for 4 weeks.

## **5.2 Evaluation of rat body, testicular, and epididymal weights subjected to various treatments**

Blood glucose levels is an indication of proper insulin function and important energy sources [44]. Insufficient insulin secretion or dysfunction of the signaling pathway results in a disturbance of glucose homeostasis. Subsequently the body will start to use other macromolecules such as lipids and proteins as sources of energy [45]. This results in shrinking of muscle tissue accompanied by a rapid weight loss in diabetic animals [45, 46]. Data from the current study showed that the body, testes, and epididymal weights were significantly lower in STZ-induced diabetic rats than the nondiabetic control group (**Figures 3–6**). These findings are in agreement with previous studies that also demonstrated a significant decrease in body, testicular, and epididymal weights in diabetic rats [5, 18, 27, 28, 33, 45, 47]. Moreover, variations in animal body and organ weights have been reported to affect spermatogenesis, sperm quality, and sperm concentration [5, 18, 27, 28, 33, 45, 47].

In the current study, diabetic animals treated with insulin improved their body and epididymal tissue weights as there was a clear regain of body weights (**Figures 3** and **4**). Synthetic insulin is a standard drug used to treat diabetes which is different from the insulin secreted naturally by the pancreas. Pancreatic insulin promotes proper metabolism, energy balance, and the maintenance of normal body weights [48]. Though the low-dose synthetic insulin used in this study had improved the weight of diabetic animals, there was still not total recovery to their normal weights.

Supplementation with KV showed similarity to the IN treatment with a significant improvement not only of the diabetic rat's body and epididymal tissue weights but also of the rat's testicular weight. Such findings are in agreement with the results of Adaramoye and Lawal [49], who reported that the treatment with KV significantly increased the weight gained by diabetic rats when compared to the untreated diabetic counterparts. Moreover, there was no significant difference in weights of nondiabetic rats supplemented with KV (N + KV) when compared to nondiabetic control group (N) (**Figures 3**–**6**). These results demonstrate that KV supplementation had no adverse effects on the animal weights confirming that the decrease observed in diabetic rats supplemented with KV was only due to their diabetic condition. This also implies that the body, testes, and epididymal weight improvement observed in the diabetic animals supplemented with KV might be due to its antioxidant and hypoglycemic potential to prevent OS and diabetes. It can be argued that the ability of KV to protect against weight loss might mainly be attributed to its glucose-lowering capacity [50]. Indeed, the regulation of glucose levels as the main source of energy by KV provides a platform for less

**307**

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced…*

**5.3 Assessment of lipid peroxidation of testicular and epididymal tissues of rats** 

MDA is an end product of LPO, and the increased levels are an indication of oxidative damage [51, 52]. It has been shown that LPO induces disturbance of fine structures; alteration of integrity, fluidity, and permeability; and functional loss of biomembranes, modifies low density lipoprotein (LDL) to proatherogenic and proinflammatory forms, and generates potentially toxic products [52]. Thus, LPO in vivo has been implicated as the underlying mechanisms in numerous disorders and diseases such as cardiovascular diseases, cancer, neurological disorders, and aging. The mechanism of free radical-mediated LPO reactions include [46] abstraction of bisallylic hydrogen from polyunsaturated fatty acids to give carbon-centered radicals which rearranges to more stable cis, trans-pentadienyl radicals [33], addition of oxygen to the pentadienyl radical to give lipid peroxyl radicals [26], release of oxygen from the peroxyl radical to give oxygen and pentadienyl radicals, which rapidly react with oxygen to give a thermochemically more stable trans, trans form preferentially than cis, trans form, and [27] intramolecular addition of the peroxyl radical to the double bond to yield bicyclic

The results clearly indicate a significantly higher and increased expression of MDA in the testicular (**Figure 7**) and epididymal (**Figure 8**) tissues of the diabetic rats when compared to the nondiabetic rats. These results are in agreement with previous study also performed on diabetic experimental animal models [49]. During diabetes, hyperglycemia causes auto-oxidation of glucose and stimulates OS through excessive free radical production. The release of free radicals causes damage to biological systems by abstracting electrons from macromolecules, thereby causing instability and disintegration [53]. For instance, peroxidation of polyunsaturated lipids on sperm membrane has been reported to cause structural alterations of the biological cell membranes as well as a change in membrane stability and function [49]. The peroxidation of sperm lipids may also disturb maturation, spermatogenesis, capacitation, acrosome reaction, and eventually membrane

In the present study, the protective mechanism of KV and IN has been examined in the onset of LPO related to STZ-induced diabetes. The findings from the study indicate that diabetic animals treated with IN recovered from LPO in the testes and epididymal tissues. This is observed through the decrease of MDA level to values

KV showed significantly healthier responses. Not only did KV supplementation significantly reduce MDA levels in the N + KV group when compared to the N group, but it also had a better effect than IN in the restoration of testicular and epididymal MDA levels of the D + KV group when compared to D only group (**Figure 7**). These findings emphasize the potentiality of KV to better restore metabolic disorders

Insulin helps to control blood glucose levels, and then this reduces the amount of free radicals released. The observed protective effects of KV in this study may be due to its antioxidant properties by scavenging the effects of hydroperoxides resulting from induced OS. This is in accordance with previous studies that have reported

use of alternative sources of energy from body, testicular, and epididymal proteins and fats. It could therefore be postulated that KV might be considered as an antidiabetic compound in the management of weight and glucose regulation in

*DOI: http://dx.doi.org/10.5772/intechopen.84822*

**subjected to various treatments**

prostaglandin-type products.

fusion, which results in male infertility [5, 6, 28–30].

close to baseline of nondiabetic rats (**Figures 7** and **8**).

related to OS such as diabetes and male infertility [5, 6, 28, 29].

diabetes.

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced… DOI: http://dx.doi.org/10.5772/intechopen.84822*

use of alternative sources of energy from body, testicular, and epididymal proteins and fats. It could therefore be postulated that KV might be considered as an antidiabetic compound in the management of weight and glucose regulation in diabetes.

## **5.3 Assessment of lipid peroxidation of testicular and epididymal tissues of rats subjected to various treatments**

MDA is an end product of LPO, and the increased levels are an indication of oxidative damage [51, 52]. It has been shown that LPO induces disturbance of fine structures; alteration of integrity, fluidity, and permeability; and functional loss of biomembranes, modifies low density lipoprotein (LDL) to proatherogenic and proinflammatory forms, and generates potentially toxic products [52]. Thus, LPO in vivo has been implicated as the underlying mechanisms in numerous disorders and diseases such as cardiovascular diseases, cancer, neurological disorders, and aging. The mechanism of free radical-mediated LPO reactions include [46] abstraction of bisallylic hydrogen from polyunsaturated fatty acids to give carbon-centered radicals which rearranges to more stable cis, trans-pentadienyl radicals [33], addition of oxygen to the pentadienyl radical to give lipid peroxyl radicals [26], release of oxygen from the peroxyl radical to give oxygen and pentadienyl radicals, which rapidly react with oxygen to give a thermochemically more stable trans, trans form preferentially than cis, trans form, and [27] intramolecular addition of the peroxyl radical to the double bond to yield bicyclic prostaglandin-type products.

The results clearly indicate a significantly higher and increased expression of MDA in the testicular (**Figure 7**) and epididymal (**Figure 8**) tissues of the diabetic rats when compared to the nondiabetic rats. These results are in agreement with previous study also performed on diabetic experimental animal models [49]. During diabetes, hyperglycemia causes auto-oxidation of glucose and stimulates OS through excessive free radical production. The release of free radicals causes damage to biological systems by abstracting electrons from macromolecules, thereby causing instability and disintegration [53]. For instance, peroxidation of polyunsaturated lipids on sperm membrane has been reported to cause structural alterations of the biological cell membranes as well as a change in membrane stability and function [49]. The peroxidation of sperm lipids may also disturb maturation, spermatogenesis, capacitation, acrosome reaction, and eventually membrane fusion, which results in male infertility [5, 6, 28–30].

In the present study, the protective mechanism of KV and IN has been examined in the onset of LPO related to STZ-induced diabetes. The findings from the study indicate that diabetic animals treated with IN recovered from LPO in the testes and epididymal tissues. This is observed through the decrease of MDA level to values close to baseline of nondiabetic rats (**Figures 7** and **8**).

KV showed significantly healthier responses. Not only did KV supplementation significantly reduce MDA levels in the N + KV group when compared to the N group, but it also had a better effect than IN in the restoration of testicular and epididymal MDA levels of the D + KV group when compared to D only group (**Figure 7**). These findings emphasize the potentiality of KV to better restore metabolic disorders related to OS such as diabetes and male infertility [5, 6, 28, 29].

Insulin helps to control blood glucose levels, and then this reduces the amount of free radicals released. The observed protective effects of KV in this study may be due to its antioxidant properties by scavenging the effects of hydroperoxides resulting from induced OS. This is in accordance with previous studies that have reported

*Antioxidants*

for 4 weeks.

45, 47].

weights.

**various treatments**

**5.1 Evaluation of induced diabetes with STZ before KV and insulin treatment**

**5.2 Evaluation of rat body, testicular, and epididymal weights subjected to** 

Blood glucose levels is an indication of proper insulin function and important energy sources [44]. Insufficient insulin secretion or dysfunction of the signaling pathway results in a disturbance of glucose homeostasis. Subsequently the body will start to use other macromolecules such as lipids and proteins as sources of energy [45]. This results in shrinking of muscle tissue accompanied by a rapid weight loss in diabetic animals [45, 46]. Data from the current study showed that the body, testes, and epididymal weights were significantly lower in STZ-induced diabetic rats than the nondiabetic control group (**Figures 3–6**). These findings are in agreement with previous studies that also demonstrated a significant decrease in body, testicular, and epididymal weights in diabetic rats [5, 18, 27, 28, 33, 45, 47]. Moreover, variations in animal body and organ weights have been reported to affect spermatogenesis, sperm quality, and sperm concentration [5, 18, 27, 28, 33,

In the current study, diabetic animals treated with insulin improved their body and epididymal tissue weights as there was a clear regain of body weights (**Figures 3** and **4**). Synthetic insulin is a standard drug used to treat diabetes which is different from the insulin secreted naturally by the pancreas. Pancreatic insulin promotes proper metabolism, energy balance, and the maintenance of normal body weights [48]. Though the low-dose synthetic insulin used in this study had improved the weight of diabetic animals, there was still not total recovery to their normal

Supplementation with KV showed similarity to the IN treatment with a significant improvement not only of the diabetic rat's body and epididymal tissue weights but also of the rat's testicular weight. Such findings are in agreement with the results of Adaramoye and Lawal [49], who reported that the treatment with KV significantly increased the weight gained by diabetic rats when compared to the untreated diabetic counterparts. Moreover, there was no significant difference in weights of nondiabetic rats supplemented with KV (N + KV) when compared to nondiabetic control group (N) (**Figures 3**–**6**). These results demonstrate that KV supplementation had no adverse effects on the animal weights confirming that the decrease observed in diabetic rats supplemented with KV was only due to their diabetic condition. This also implies that the body, testes, and epididymal weight improvement observed in the diabetic animals supplemented with KV might be due to its antioxidant and hypoglycemic potential to prevent OS and diabetes. It can be argued that the ability of KV to protect against weight loss might mainly be attributed to its glucose-lowering capacity [50]. Indeed, the regulation of glucose levels as the main source of energy by KV provides a platform for less

were confirmed by hyperglycemia after 4 days and maintained

In the current study, the single intraperitoneal administration of STZ (50 mg/kg) in adult Wistar rats was effective in causing hyperglycemia after 5 days. This was confirmed by the significantly higher plasma glucose levels (18 mmol/l, see **Figure 3**) in the STZ group of animals which is typical of type 1 diabetes mellitus. It was therefore concluded that the diabetic animal model was successfully created and the results were similar to and supported by previous findings [42, 43] where induction of DM in Wistar rats via intravenous STZ injection (of 40 and 45 mg/kg/b.w, respectively)

**306**

the beneficial effects of KV against testicular damage induced by various chemicals [2, 5, 6, 28–30, 33, 35].

## **5.4 Assessment of antioxidant enzymes in the testicular and epididymal tissues to various treatments**

Antioxidant enzymes such as SOD, CAT, and GPX play a crucial role in protecting the testes and epididymal tissues against OS associated damage and male reproductive disorders [43–45].

Physiological and pathophysiological conditions such as diabetes influence the level of production and activity of these antioxidant enzymes [2, 6]. The reduction in antioxidant enzymes has been previously reported in diabetic animals [20]. The observed reduction in antioxidant enzyme activities could be due to the oxidative inactivation of the enzyme by ROS or by the glycation of the enzymes [20, 45]. The reduced activity of SOD, CAT, and GPX in the epididymal and testicular tissues has been observed following STZ induction of diabetes, and this may result in a number of deleterious effects due to the accumulation of superoxide radicals and H2O2.

In epididymal tissue the SOD activity was significantly lower in STZ-induced diabetic rats when compared to nondiabetic control rats (**Table 1**). This is in agreement with a study by Adaramoye and Lawal [49] who demonstrated that a diabetogenic agent reduced SOD activity in epididymal tissue. Both catalase and GPx activities in the testes and epididymis were significantly lower in STZ-induced diabetic rats than in the nondiabetic control rats. Glutathione peroxidase shares the substrate, H2O2, with CAT; it alone can react effectively with lipids and other organic hydroperoxides, being the major source of protection against low levels of OS. Some authors supported the idea that GPx was essential in the protection against OS under normal conditions [54]. Others believed in a protective role for these enzymes only under OS conditions [2]. Generally, in our study, the activity of testicular and epididymal antioxidant enzymes SOD, CAT, and GPx was depleted in diabetic rats. Diabetes-induced tissue OS is further supported by the elevated levels of MDA.

Numerous compounds with antioxidant activities have been shown to improve or normalize the activities of antioxidant enzymes in nondiabetic and diabetic rats, respectively [4]. In the present study, the supplementation of KV for 6 weeks to the normal rats did not change SOD, CAT, and GPx activities compared to the nondiabetic rats. This might be due to the interference between natural antioxidants produced by the body and the antioxidant effects of KV. The treatment of STZ-induced diabetic rats with KV influenced the activity of SOD, CAT, and GPx compared to the diabetic groups (**Table 1**). Similarly, to previous studies, the supplementation of dietary antioxidants to experimental animals has shown a positive correlation between natural dietary supplementation and increased antioxidant enzyme levels in induced OS models. In other studies, KV restored antioxidant enzymes in the testes of diabetes-induced rats [5, 49]. The protective effect of KV observed in the testes and epididymis of diabetic rats might either be due to the inhibition of glycation by the antioxidant enzymes or scavenging abilities of ROS, thus decreasing the formation of LPO [5, 27–30].

Insulin has been used in the management of diabetes by restoring pancreatic insulin deficiency. From our results it is clear that synthetic insulin had improved the levels of testicular and epididymal antioxidant enzymes in STZ-induced diabetic rats. These results confirm the central role of insulin in energy homeostasis and also make it an important signaling factor in the reproductive tract [2, 7]. The observed effects of KV on the testes and epididymis of STZ-induced diabetic rats in the present study could be attributed to its hypoglycemic and antioxidant properties.

**309**

provided the original work is properly cited.

Claudine Manirafasha1,2, Omolola Rebecca Oyenihi1

and Yapo Guillaume Aboua4

Peninsula University of Technology, Cape Town, South Africa

University of Science and Technology, Windhoek, Namibia

\*Address all correspondence to: yaboua@nust.na

1 Faculty of Health and Wellness Sciences, Cape Peninsula University of

2 Division of Medical Physiology, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa

3 Department of Wellness Sciences, Faculty of Health and Wellness Sciences, Cape

4 Department of Health Sciences, Faculty of Health and Applied Sciences, Namibia

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

, Nicole Lisa Brooks3

\*

,

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced…*

The findings of this study emphasized the protective effects of KV against diabetes-associated OS in the testicular and epididymal tissues by enhancing antioxidant defense system in STZ-induced diabetic rats. The present study showed that that KV has the potential of being used as a treatment for diabetes-related pathologies and their complications especially testicular dysfunction. We propose further investigations to elucidate the effects of KV on male reproductive organ function in order to advance the current knowledge which could also be extended to

*DOI: http://dx.doi.org/10.5772/intechopen.84822*

**6. Conclusion**

clinical research.

**Author details**

Stefan S. du Plessis2

Technology, Bellville, South Africa

*Potential Antioxidative Effects of Kolaviron on Reproductive Function in Streptozotocin-Induced… DOI: http://dx.doi.org/10.5772/intechopen.84822*
