褪黑素在活性氧致精子线粒体功能损伤中的保护作用

目的 :探讨活性氧 (ROS)对精子线粒体功能的损伤以及褪黑素 (MLT)的保护作用。　方法 :采用Percoll梯度离心法选择具有正常生理功能的精子 ,作为本实验的正常精子模型。应用次黄嘌呤—黄嘌呤氧化酶体系产生ROS ,在MLT存在与不存在情况下 ,与精子模型分别孵育 30和 6 0min后 ,采用酶组织化学方法分析精子线粒体部位的琥珀酸脱氢酶 (SDH)活性 ,采用Rhodamine 1 2 3(Rh1 2 3)荧光探针标记精子 ,通过流式细胞仪检测线粒体膜电位。　结果 :正常精子与ROS孵育后 ,精子线粒体膜电位明显降低 ,线粒体SDH活力降低极为显著 ;而MLT则减轻了ROS对精子线粒体功能的损伤。　结论 :ROS可通过对精子线粒体膜电位和SDH活力的影响 ,而导致精子线粒体功能损伤 ;MLT可通过其有效的抗氧化能力 ,保护精子对抗ROS对其线粒体功能的损伤     

人精子体外氧化损伤对线粒体tRNA~(LeuUUR)基因的影响

目的:探讨活性氧(ROS)对人类精子线粒体tRNALeuUUR基因的氧化损伤。方法:采用Percoll梯度离心法筛选具有正常生理功能的精子,作为正常精子模型,并分为损伤组20例和对照组20例,分别加入次黄嘌呤-黄嘌呤氧化酶体系或不予处理,37℃有氧环境中孵育60min。分别提取精子DNA,以Fpg酶切损伤碱基并采用接头介导PCR(LM-PCR)检测线粒体tRNALeuUUR基因的氧化损伤。采用Rhodamine(Rh123)荧光探针标记精子,通过流式细胞仪检测线粒体膜电位,观察精子的功能。结果:与对照组相比,损伤组精子孵育后线粒体膜电位明显降低[(116.27±11.72)%vs(64.00±4.88)%,P<0.05]。Fpg酶切和LM-PCR显示精子线粒体tRNALeuUUR基因损伤。结论:ROS可能通过对精子线粒体tRNALeuUUR基因氧化损伤而影响精子功能(线粒体膜电位明显降低),从而引起不育。     

活性氧致人精子运动功能和存活力变化的分析

目的 :对活性氧 (ROS)作用后精子的运动参数和存活率的变化进行分析 ,以证实ROS是否为引起精子运动功能障碍的病因之一。　方法 :采用Percoll梯度离心法选择具有正常生理功能的人精子作为正常精子模型 ,应用次黄嘌呤 黄嘌呤氧化酶体系产生ROS ,在有氧环境下与精子模型孵育后 ,运用计算机辅助精液分析 (CASA)系统 ,分析ROS攻击后精子运动参数的改变。　结果 :与对照组相比 ,正常精子模型与ROS孵育 30min后 ,精子活动率、曲线速度 (VCL)、直线速度 (VSL)、平均路径速度 (VAP)均明显下降 (P <0 .0 0 1) ,头侧摆幅度 (ALH)尚无明显改变 (P >0 .0 5 ) ,而与ROS孵育 6 0min后 ,精子运动功能近乎丧失 ,精子主要运动参数趋向于零。　结论 :ROS与正常精子作用后 ,可导致精子运动功能下降 ,从而证实ROS为精子运动功能障碍的病因之一。     

正常精子体外与活性氧作用后超微结构观察

目的 :观察精子与活性氧 (ROS)作用后超微结构变化。　方法 :采用Percoll梯度离心法选择具有正常生理功能的精子作为正常精子模型 ,应用次黄嘌呤 黄嘌呤氧化酶体系产生ROS ;在有氧环境下ROS与精子模型孵育后 ,采用透射电镜观察精子超微结构。　结果 :正常精子模型与ROS作用后 ,精子膜及顶体存在不同程度的损伤 ,精子线粒体结构出现异常。　结论 :过多的ROS可致精子膜、顶体以及线粒体的超微结构改变 ,损害精子功能。     

Effects of reactive oxygen species from activated leucocytes on human sperm motility, viability and morphology

The accumulated data suggest that inflammation can increase the level of reactive oxygen species (ROS), which contribute to impaired sperm function and male infertility. Therefore, we propose that inflammation-mediated production of ROS in male and female reproductive tracts hinder sperm fertilisation. To test this hypothesis, phorbol myristate acetate (PMA) with polymorphonuclear leucocytes (PMNs) was applied to generate endogenous ROS. We evaluated the time-dependent effects of ROS on human sperm motility, viability and mitochondrial membrane potential (MMP). The results showed that after treatment with PMA and PMNs, the motility of human spermatozoa significantly decreased to 50% on Day 1 and 15% on Day 4 compared with that of the, respectively, negative controls (P = 0.012). The viability of human spermatozoa decreased on Day 4 of PMA + PMNs treatment (P = 0.028). The MMP of human spermatozoa significantly decreased from Day 2 to Day 4 in the PMA + PMN group compared with that of the controls (P = 0.019). Taken together, the 4-day cultivation approach provided an accurate evaluation of sperm quality, especially sperm motility and MMP. Our findings indicated that endogenous inflammation increased ROS levels, which might induce sperm oxidative damage. Additionally, sperm motility might be one of the earliest and most sensitive indicators of this damage.     

The effect of cysteine and glutamine on human sperm functional parameters during vitrification

Assuming the adverse effects of reactive oxygen species (ROS) on sperm function, this study was conducted to assess the effects of cysteine and glutamine as effective antioxidants on human sperm parameters under vitrification. Twenty normozoospermic samples were used. The samples were subjected to a vitrification process and cysteine (5 and 10 mM) and glutamine (10 and 15 mM). The sperm motility parameters, mitochondrial membrane potential (MMP), plasma membrane integrity (PMI), DNA damage and intracellular ROS damage were assessed for each sample. Statistical analyses showed that motility, mitochondrial membrane potential and DNA damage decreased in the vitrified groups with cysteine 5, 10 mM and glutamine 10, 15 mM separately. Also intracellular ROS increased significantly compared to the fresh group (p < .05). No significant differences were observed for PMI compared with the fresh group (p > .05). Supplementation of cysteine and glutamine in both concentrations separately decreased intracellular ROS and DNA damage of spermatozoa with significant increase in PMI, MMP and progressive motility compared to vitrified control group (p < .05). The results showed no significant effect of a specific concentration in cysteine and glutamine on sperm parameters compared to other concentrations. Both amino acids have the potential to improve the harmful effects of freezing on sperm parameters.     

Antioxidant effects of penicillamine against in vitro-induced oxidative stress in human spermatozoa

Oxidative stress contributes importantly to the aetiology of male infertility, impairing sperm function. The protective effect of antioxidants on seminal parameters has been established, and the antioxidant penicillamine has shown beneficial effects; however, its protective effect on human spermatozoa exposed to oxidative stress has not been reported. The objective of this work was to evaluate the effect of penicillamine on human spermatozoa exposed in vitro to oxidative stress. First, the effect of penicillamine on spermatozoa from normozoospermic donors was evaluated. Then, the effect of penicillamine on spermatozoa exposed to oxidative stress induced separately by ionomycin and hydrogen peroxide (H₂O₂) was analysed. An untreated control and a control treated only with the oxidative stress inducer were included. Reactive oxygen species (ROS) levels, viability, mitochondrial membrane potential (MMP) and motility were analysed. The results showed that penicillamine, added to the incubation medium, decreased the ROS levels induced by ionomycin and H₂O₂, and this effect was associated with better preservation of MMP, motility, and ATP levels. These results highlight the potential advantages of penicillamine supplementation of sperm culture medium, especially for semen samples with high ROS levels and also in circumstances where laboratory handling can cause an increase in ROS production.     

Effects of semen processing on the generation of reactive oxygen species and mitochondrial membrane potential of human spermatozoa

This study was designed to evaluate the effects of semen processing on the generation of intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) in spermatozoa, and to develop reliable indexes for the evaluation of sperm quality during sperm preparation. Swim-up and density gradient centrifugation methods were used to separate semen in oligoasthenoteratozoospermia (OAT), leucocytospermia (LC) and normozoospermia groups. Levels of ROS and MMP were measured by flow cytometry. Before preparation, the patients with abnormal semen parameters had a lower MMP and higher ROS, and there was a negative correlation between MMP and ROS. The levels of MMP and ROS increased significantly, especially ROS produced by swim-up. A significant difference was found between the correlation of MMP and total normal motile sperm count after preparation in the OAT group. The level of ROS was associated with the amount of white blood cells in the LC group. The MMP can be used as an objective index to evaluate the sperm quality of OAT patients, and the combination of MMP and ROS can be used to assess the efficiency of sperm preparation in LC patients. These findings can guide selection of the ideal sperm separation technique for different sperm samples.     

Effect of mitochondrial calcium uniporter blocking on human spermatozoa

Calcium (Ca²⁺) regulates a number of essential processes in spermatozoa. Ca²⁺ is taken up by mitochondria via the mitochondrial calcium uniporter (mCU). Oxygen‐bridged dinuclear ruthenium amine complex (Ru360) has been used to study mCU because it is a potent and specific inhibitor of this channel. In bovine spermatozoa, it has been demonstrated that mitochondrial calcium uptake inhibition adversely affects the capacitation process. It has been demonstrated in human spermatozoa that mCU blocking, through Ru360, prevents apoptosis; however, the contribution of the mCU to normal human sperm function has not been studied. Therefore, the aim of this study was to evaluate the effect of mCU blocking on human sperm function. Spermatozoa obtained from apparently healthy donors were incubated with 5 and 10 μm Ru360 for 4 h at 37 °C. Viability was assessed using propidium iodide staining; motility was determined by computer‐aided sperm analysis, adenosine triphosphate (ATP) levels using a luminescence‐based method, mitochondrial membrane potential (ΔΨm) using JC‐1 staining and reactive oxygen species (ROS) production using dihydroethidium dye. Our results show that mCU blocking significantly reduced total sperm motility and ATP levels without affecting sperm viability, ΔΨm and ROS production. In conclusion, mCU contributes to the maintenance of sperm motility and ATP levels in human spermatozoa.     

The mitochondria of stallion spermatozoa are more sensitive than the plasmalemma to osmotic-induced stress: role of c-Jun N-terminal kinase (JNK) pathway

Cryopreservation introduces extreme temperature and osmolality changes that impart lethal and sublethal effects on spermatozoa. Additionally, there is evidence that the osmotic stress induced by cryopreservation causes oxidative stress to spermatozoa. The main sources of reactive oxygen species in mammalian sperm are the mitochondria. In view of this, the aim of our study was to test whether or not osmotic stress was able to induce mitochondrial damage and to explore the osmotic tolerance of the mitochondria of stallion spermatozoa. Ejaculates from 7 stallions were subjected to osmolalities ranging from 75 to 1500 mOsm/kg, and the effect on sperm membrane integrity and mitochondrial membrane potential was studied. Additionally, the effects of changes in osmolality from hyposmotic to isosmotic and from hyperosmotic to isosmotic solutions were studied (osmotic excursions). The cellular volume of stallion spermatozoa under isosmotic conditions was 20.4 ± 0.33 μm(3). When exposed to low osmolality, the stallion spermatozoa behaved like a linear osmometer, whereas exposure to high osmolalities up to 900 mOsm/kg resulted in decreased sperm volume. Although sperm membranes were relatively resistant to changes in osmolality, mitochondrial membrane potential decreased when osmolalities were low or very high (10.7 ± 1.74 and 16.5 ± 1.70 at 75 and 150 mOsm/kg, respectively, and 13.1 ± 1.83 at 1500 mOsm/kg), whereas in isosmolar controls the percentage of stallion sperm mitochondria with a high membrane potential was 41.1 ± 1.69 (P < .01). Osmotic excursions induced greater damage than exposure of spermatozoa to a given nonphysiologic osmolality, and again the mitochondria were more prone to damage induced by osmotic excursions than was the sperm plasma membrane. In search of intracellular components that could mediate these changes, we have detected for the first time the c-Jun N-terminal kinase 1/2 in stallion spermatozoa, which are apparently involved in the regulation of the viability of these cells.     

The effect of reactive oxygen species on equine sperm motility, viability, acrosomal integrity, mitochondrial membrane potential, and membrane lipid peroxidation

The objective of this study was to examine the influence of reactive oxygen species (ROS), generated through the use of the xanthine (X)-xanthine oxidase (XO) system, on equine sperm motility, viability, acrosomal integrity, mitochondrial membrane potential, and membrane lipid peroxidation. Equine spermatozoa were separated from seminal plasma on a discontinuous Percoll gradient, and spermatozoa were incubated with 0.6 mM X and 0.05 U/mL XO for 30 minutes. Catalase (150 U/mL), superoxide dismutase (SOD, 150 U/mL), or glutathione (GSH, 1.5 mM) were evaluated for their ability to preserve sperm function in the presence of the induced oxidative stress. At the end of the 30-minute incubation, sperm motility was determined by computer-assisted semen analysis. Viability and acrosomal integrity were determined by Hoechst-Pisum sativum staining, and mitochondrial membrane potential was determined by staining with JC-1. Incubation with the X-XO system led to a significant (P < .01) increase in hydrogen peroxide production and an associated decrease (P < .01) in motility parameters. Total motility was significantly (P < .01) lower in the presence of X-XO compared with the case of the control (29%+/-9% vs 73%+/-1%, respectively). Catalase, but not SOD, prevented a decline in motility secondary to oxidative stress (71%+/-4% vs 30%+/-3%, respectively). The addition of glutathione had an intermediate effect in preserving sperm motility at the end of the 30-minute incubation (53%+/-3%). No influence of X-XO could be determined on viability, acrosomal integrity, or mitochondrial membrane potential. In order to promote lipid peroxidation, samples were incubated with ferrous sulfate (0.64 mM) and sodium ascorbate (20 mM) for 2 hours after the X-XO incubation. No increase in membrane lipid peroxidation was detected. This study indicates that hydrogen peroxide is the major ROS responsible for damage to equine spermatozoa. The decrease in sperm motility associated with ROS occurs in the absence of any detectable decrease in viability, acrosomal integrity, or mitochondrial membrane potential or of any detectable increase in lipid peroxidation.     

Comparative study of fertility parameters in vitrified human spermatozoa in the presence or absence of EmbryORP®: A novel antioxidant

The cryopreservation of spermatozoa has the main purpose of preserving male fertility. However, current preservation techniques have shown to produce lesions in the structure and alter sperm functions, probably due to the production of reactive oxygen species (ROS) during cryopreservation. To overcome the damage provoked by ROS, we introduced a novel antioxidant called EmbryORP^® in a vitrification protocol and compared eight fertility parameters: motility, viability, morphology, concentration, the semen pH, the oxidation-reduction potential (ORP), the spontaneous acrosomal reaction (AR) and the mitochondrial membrane potential (MMP), in the presence or absence of EmbryORP^®. We analysed 20 samples from healthy human sperm donors and observed that the antioxidant significantly decreased the semen pH as well as the MMP and the ORP affecting the balance of ROS. The antioxidant also lowered the motility and viability of the cells, but preserved the acrosome and sperm morphology in general. We concluded that EmbryORP^® lowered the ORP, but to a suboptimal level that may be harmful to spermatozoa. Despite these results, our work opens new perspectives on how to improve cryopreservation media. Therefore, we recommend exploring the EmbryORP^® potential benefit by reducing its concentration or changing the exposure time during the cryopreservation protocol.     

Analysis of the Changes of Movement Function and Viability in Human Spermatozoa Induced by Reactive Oxygen Species

Objective: To study the influence of reactive oxygen species (ROS) on the mobility and viability of human spermatozoa. Methods: Spermatozoa with normal function were selected from human semen samples by the Percoll gradient centrifugation technique. ROS were generated by the hypoxanthine-xanthine oxidase system and were incubated with the spermatozoa under aerobic environment. Movement parameters of spermatozoa were analyzed by the computer-assisted semen analysis (CASA) system. Results: Thirty min after incubation with ROS, the motility, curvilinear velocity (VCL), straight line velocity (VSL) and average path velocity (VAP) of the spermatozoa were significantly decreased (P<0.01), while the change in the amplitude of lateral head displacement (ALH) was insignificant (P>0.05). After 60 min incubation, the motility was almost lost with all the movement parameters close to zero. Conclusion: When normal spermatozoa were incubated with ROS, the mobility was decreased. It is believed that ROS may be one of t     

The restoration of kidney mitochondria function by inhibition of angiotensin-II production in rats with acute adriamycin-induced nephrotoxicity

Adriamycin (ADR) is commonly used for many solid tumor treatments. Its clinical utility is, however, largely limited by the adverse reactions, are known to be nephrotoxic. The mechanism by which it induces kidney damage is still not completely understood, but its nephrotoxicity might relate to increase reactive oxidant status (ROS), mitochondrial dysfunction. Until now, neurohormonal activation of it is unclear. ADR might activate the renin angiotensin system. Angiotensin-II also induced ROS and mitochondrial dysfunction. The aim of this study was to investigate whether angiotensin-II production inhibition has the protective effect on attenuation of mitochondrial function in rats with acute ADR-nephrotoxicity or not. Rats were divided into five groups as a control, ADR, co-treated ADR with captopril (CAP), co-treated ADR with Aliskren, co-treated ADR with both CAP and Aliskren groups. Creatinine kinase (CK) levels were measured at the end of treatment period. The kidneys were homogenized and biochemical measurements were made in mitochondria, cytosol. Mitochondria membrane potential (MMP) and ATP levels were determined. ADR increased CK levels and oxidative stress in mitochondria too (p?0.05). ADR significantly decreased MMP and ATP level in kidney mitochondria (p?0.05). Co-administration with ADR and Aliskren and CAP improved the dissipation of MMP (p?0.05). The decrease in ATP level was restored by treatment with inhibitors of ACE and renin. We concluded that inhibitors of angiotensin-II are effective against acute ADR induced nephrotoxicity via the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.     

精子线粒体琥珀酸脱氢酶的检测及意义

目的 :采用一种简便、快速的检测精子线粒体琥珀酸脱氢酶 (SDH)的改良方法检测精子SDH ,并评价其与精子活动率及存活率的关系。　方法 :4 6例年龄为 2 5～ 36岁 (平均 31岁 )生育与不育男性精液标本 ,采用计算机辅助精液分析系统检测精子活动率 ,应用改良SDH检测法检测精子SDH ,通过死、活精子荧光分子探针染色检测精子存活率 ,分析精子活动率、存活率及精子SDH阳性率之间的关系。　结果 :4 6例生育与不育男性精子活动率为( 6 7.33± 7.37) % ,存活率为 ( 79.78± 7.6 5 ) % ,精子SDH阳性率为 ( 74 .74± 8.2 9) % ;精子活动率、存活率及精子SDH阳性率 3者之间均存在显著相关性 (P均 <0 .0 1)。　结论 :精子线粒体SDH检测对评价精子线粒体功能具有重要意义 ,还可作为精子存活率的辅助指标     

五子衍宗丸对少弱精子症模型大鼠精子线粒体膜电位及超微结构影响

目的:研究五子衍宗丸对少弱精子症模型大鼠精子线粒体膜电位(MMP)水平及线粒体超微结构的影响。方法:取体重为200～220 g雄性SD大鼠60只,随机分成正常组,模型组,对照组(黄精赞育胶囊组),五子衍宗丸低、中、高剂量组,除正常组外,其他各组大鼠灌服雷公藤多苷[30 mg/(kg.d)],连续8周,制备少弱精子症模型。造模结束后,正常组、模型组给予等容量蒸馏水[10 ml/(kg.d)],对照组给予黄精赞育胶囊溶液[3.01 g/(kg.d)],五子衍宗丸各组分别给予水提液,低剂量组[2.30 g生药/(kg.d)],中剂量组[4.60 g生药/(kg.d)],高剂量组[9.20 g生药/(kg.d)],连续30 d。末次给药后30 min,采用荧光流式细胞技术(JC-1染色)测定精子MMP水平(JC-1+%),并通过透射电镜观察精子线粒体超微结构的改变。结果:①MMP:JC-1+%和强度分别为:正常组70.80±4.92、4 360±945;模型组33.77±6.19、1 4685±496;对照组56.34±10.35、3 277±895;五子衍宗丸低剂量组40.80±10.40、2 016±767;中剂量组59.40±6.51、3 897±643;高剂量组60.71±7.81、3 371±6467。造模各组大鼠精子线粒体JC-1+%及强度均明显下降,与正常组比较差异有显著性意义(P均<0.05);连续给药30 d后,给药各组均能明显提高精子MMP,增加JC-1+%,除低剂量组外,其他用药各组与模型组比较差异有显著性意义(P均<0.05)。②精子线粒体超微结构:雷公藤造模后,精子外膜松散、变性,线粒体肿胀、大小不一、线粒体膜不完整,轴丝结构不清或出现断裂。给予五子衍宗丸30 d后,精子外膜及线粒体膜结构完整,减少线粒体肿胀,轴丝及微管结构基本正常。结论:雷公藤多苷能降低精子MMP水平,破坏线粒体的结构。五子衍宗丸能明显提高少弱精子症模型大鼠精子MMP水平,减轻精子线粒体结构损伤。保护精子线粒体结构与功能的完整是五子衍宗丸治疗少弱精子症的机制之一。     

冻存后大鼠精子活力变化与其结构的关系

目的　观察冷冻对大鼠精子活动能力的影响 ,并探讨其活动能力的变化与细胞膜完整性、DNA结构、线粒体鞘和顶体的关系。　方法　使用计算机辅助精子活动分析仪 (CASA)检测冻存前后大鼠精子活动力的变化 ;荧光素乙酰乙酸盐 (FDA)染色法检测大鼠精子细胞膜的完整性 ;双氢鲁丹明荧光反应观察精子线粒体鞘的变化 ;金霉素 (CTC)荧光检测法观察冻存对大鼠精子顶体的影响。　结果　复苏后精子的活动力下降 ,为冻存前的 39.7% ;FDA检测显示冻存后的大鼠精子细胞膜完整 ,未受到破坏 ;冻存后的大鼠精子线粒体鞘荧光强度下降 ,且荧光不连续、甚至消失 ;CTC荧光反应显示冻存后精子顶体反应 (AR)的类型发生改变 ,AR型精子比例明显下降 ,由冻存前的 6 8.6 %降至冻存后的 13.4 %。　结论　冻存后大鼠精子细胞膜的完整性未受到破坏 ;精子的线粒体鞘和顶体受到较明显的破坏。大鼠精子冻存复苏后活力下降与线粒体鞘和AR存在相关性。     

Aquaporin3 expression and the potential role of aquaporins in motility and mitochondrial membrane potential in human spermatozoa

Aquaporins are water selective channels which play important roles in cell volume regulation during the transmission of spermatozoa to female tract. This study investigated the expression of aquaporin3 and determined the role of aquaporins in human sperm motility and mitochondrial membrane potential (MMP). RT-PCR and flow cytometry analysis were done to investigate aquaporin3 expression levels, and immunolocalisation of aquaporin3 in the spermatozoa was detected using immunocytochemical analysis. The sperm suspension was divided into four groups of spermatozoa: (a) Spermatozoa at 0 hr, (b) spermatozoa in control group, (c) spermatozoa treated with HgCl₂ (as an aquaporin inhibitor) and (d) spermatozoa treated with HgCl₂+ and 2-mercaptoethanol. The sperm samples were examined in terms of sperm motility and mitochondrial membrane potential. Results confirmed aquaporin3 expression in human spermatozoa and immunocytochemistry results showed an intense immunoreactivity in whole sperm tail. After 60 min, HgCl₂ showed a significant decrease in motility and MMP compared to the control group. At this time point, 2-mercaptoethanol in the HgCl₂+ 2-mercaptoethanol group reversed the effects of HgCl₂ as compared to the HgCl₂ group. Present study showed the expression and immunolocalisation of AQP3 in human spermatozoa and the potential role of AQPs in the sperm motility and MMP.     

Detection of "apoptosis-like" changes during the cryopreservation process in equine sperm

The kinematics of the appearance of apoptotic markers was studied by flow cytometry and immunoblot assays in equine spermatozoa subjected to freezing and thawing. Caspase activity, low mitochondrial membrane potential, and increases in sperm membrane permeability were observed in all of the phases of the cryopreservation procedure. Freezing and thawing caused an increase in membrane permeability and changes in the pattern of caspase activity; decreases in mitochondrial membrane potential were observed after centrifugation and cooling to 4 degrees C and after freezing and thawing. It is proposed that sperm mitochondria may be directly involved in the subtle damage that is present in most spermatozoa surviving freezing and thawing.     

Causes and consequences of sperm mitochondrial dysfunction

Mitochondria have multiple functions, including synthesis of adenine triphosphate, production of reactive oxygen species, calcium signalling, thermogenesis and apoptosis. Mitochondria have a significant contribution in regulating the various physiological aspects of reproductive function, from spermatogenesis up to fertilisation. Mitochondrial functionality and intact mitochondrial membrane potential are a pre-requisite for sperm motility, hyperactivation, capacitation, acrosin activity, acrosome reaction and DNA integrity. Optimal mitochondrial activity is therefore crucial for human sperm function and semen quality. However, the precise role of mitochondria in spermatozoa remains to be fully explored. Defects in sperm mitochondrial function severely impair the maintenance of energy production required for sperm motility and may be an underlying cause of asthenozoospermia. Sperm mtDNA is susceptible to oxidative damage and mutations that could compromise sperm function leading to infertility. Males with abnormal semen parameters have increased mtDNA copy number and reduced mtDNA integrity. This review discusses the role of mitochondria in sperm function, along with the causes and impact of its dysfunction on male fertility. Greater understanding of sperm mitochondrial function and its correlation with sperm quality could provide further insights into their contribution in the assessment of the infertile male.