Management of idiopathic oligoasthenospermia with lycopene

NK Mohanty; Sujit Kumar; AK Jha; RP Arora

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ORIGINAL ARTICLE

Year : 2001 \| Volume : 18 \| Issue : 1 \| Page : 57-61

Management of idiopathic oligoasthenospermia with lycopene

NK Mohanty, Sujit Kumar, AK Jha, RP Arora
Department of Urology, Safdarjang Hospital, New Delhi, India

Correspondence Address:
N K Mohanty
D-II/87, West Kidwai Nagar, New Delhi - 110 023
India

Source of Support: None, Conflict of Interest: None

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Abstract

Idiopathic oligoasthenosperinia accounts. for almost 24% of all male infertility. The role of free radicals as a cause of such male infertility has been established recently. We undertook a study to establish the role of Lycopene (antioxidant) in management of such infertile males due to free radicals.
A total number of 50 patients having no obvious cause for their infertility with normal hormone profile and antisperin antibody titre but showing oligoasthenospermia were given Lycopene (Lycored) 8 mg daily till their sperm analysis improved to optimal level or pregnancy was achieved. Regular, follow-up for one year with sperm analysis was done.
Result showed a 36% pregnancy rate with improvement of sperm count and functional sperm concentration in 70% and 60% respectively, sperm motility and sperm motility index improved in 54% and 46% while 38% showed improvement in sperm morphology. There were no side effects with good patient compliance.
Conclusion: Lycopene supplementation has a definite role in management of idiopathic oligoasthenospermia.

Keywords: Lycopene; Antioxidant: Oligoasthenospermia: Motility: Idiopathic

How to cite this article:
Mohanty N K, Kumar S, Jha A K, Arora R P. Management of idiopathic oligoasthenospermia with lycopene. Indian J Urol 2001;18:57-61

How to cite this URL:
Mohanty N K, Kumar S, Jha A K, Arora R P. Management of idiopathic oligoasthenospermia with lycopene. Indian J Urol [serial online] 2001 [cited 2021 Mar 1];18:57-61. Available from: https://www.indianjurol.com/text.asp?2001/18/1/57/37419

Introduction

Impaired sperm function is an obvious and general cause of male idiopathic infertility.[1] Idiopathic male infertility accounts for almost 24% of all male infertility cases. Though their antisperm antibody titre and hormone profile are well within normal values but their seminalogram shows either oligospermia. asthenospermia or tetraspermia.

One of the most common abnormalities associated with male infertility is the presence of free radicals in their ejaculate. These free radicals damage the sperm's structure and DNA material. (Brit Scientific & Med; Nov 1998)

Oxidative stress status (OSS) resulting in production of excessive reactive oxygen species (ROS) is now considered to be the causative factor for sperm damage, low sperm count and sluggish motility leading to idiopathic male infertility. Uncontrolled and excessive production of free radicals have a significant role as one of the major factors leading to infertile males.[2],[3],[4],[5],[6] Studies have shown that 40-80% of non selected infertile patients have high levels of seminal free oxygen radical.[7] Infertile men have higher free radicals than fertile men. (Centre for Male Reprod Med)

Human spermatozoa are rich in poly unsaturated fatty acid (PUFA) and therefore are susceptible to free radical attack mediated by lipid peroxidation.[8],[9]

Free radicals can be detected in the semen of 40% of infertile men. whereas none is detected in semen from fertile men. (Ind Jr of Androl; 1993)

Excessive free radicals are related to an increase in lipid peroxidation of sperm cell. Lipid peroxides damage proteins by oxidation of critical - SH group in proteins and DNA which alter the structure and function of spermatozoa.

To counteract the harmful effects of ROS, sperm and seminal plasma possess a number of antioxidant systems that scavenges ROS and prevents internal cellular damage.[10],[12],[13]

A prospective study has demonstrated that men with high levels of free radical (FR) generation have sevenfold less chance of initiating a pregnancy as compared with those with low free radicals.[10] Free radicals causing male infertility by affecting the process of conception at various stages like damage to sperm membrane, DNA and protein resulting in decreased sperm count, mortility, viability and increased mid piece defect that impairs sperm capacitation and acrosome reaction.[14],[15],[16]

Studies have shown infertile males have elevated levels of free radical induced DNA damage in their ejaculated spermatozoa[17] and also 8-hydroxydeoxyguanosine.[18] Recent research have shown OSS results in sperm DNA fragmentation.[19] Lipid peroxides are highly toxic to speniiatozoa and causes reversible arrest of motility[8],[20],[21] resulting in tetraspermia.

High levels of FR block the sperm motility though the inhibition of ATP synthesis by the mitochondria enzyme and cell membrane compounds injury.[22],[23] Research have shown high levels of free radicals induce reversible anxonemal damage and sperm immobilization[24] mostly due to depletion of ATP and insufficient axonemal protein phospherylation and decreased capacity for sperm oocyte fusion.[25],[26],[27] A negative correlation is observed in spermoocyte fusion due to FR.[20],[25],[26],[27]

Infection of male genitalia like prostatitis, epididymorchitis and seminal vesiculitis result in production of more free radicals resulting in harmful effects on spermatozoa.[28] The level of Lycopene was significantly decreased in seminal plasma of infertile males.

Therefore free radicals cause infertility by affecting the process of spermatogenesis at different levels like sperm membrane damage, sperm protein damage and sperm DNA damage through lipid peroxidation.[29]

The role of FR as a cause of idiopathic male infertility is getting a lot of attention and more and more studies today confirm this hypothesis. Depressed seminal antioxidant capacity have been implicated in male infertility. Both total antioxidant capacity (TAC) and individual antioxidant levels have been shown to be lower in the serum of infertile males.[4],[10],[11]

Studies have shown that pre treatment with antioxidants that dispose, scavenge and suppress this formation of free radicals can reduce DNA damage.[30]

Among well known biological antioxidants, super oxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH) have a significant role in protecting the sperm against peroxidase damage.[31],[32] Therefore antioxidant therapy can be considered for idiopathic infertile males.[33],[34] Another study[35] has shown that restoration of antioxidants defence might prove useful for invigorating the physiological function of sperm.

Furthermore studies on infertile males empirically treated with antioxidant have demonstrated improved semen characted stics[36],[37],[38],[39] with higher rate of pregnancy.

Lycopene is one of the 650 different carotenoids naturally synthesised and found in fruits and vegetables. Lycopene is the most potent quencher of FR in our redox defence against FR[39],[40] It plays a major role in management of male infertility due to oligoasthenospermia.

The aim of our study is to assess the role of Lycopene supplementation in treating patients with idiopathic male infertility due to oligoasthenospermia.

Materials and Methods

50 infertile males having normal hormone profile, antisperm antibody titre, but oligoasthenospermic were included in our study with the following inclusion criteria.

Age between 21 to 50 years.
Sperm count less than 50 million/cu.mm.
Sperm motility less than 50%.
Sperm morphology (normal) less that 50%
Sperm motility index less than 80.
Functional sperm count less than 3 million/cu.mm.
No history of taking any therapy for their infertility.
No history of obstructive azoospermia
Normal female partner
A written consent

With the above inclusion criteria all these 50 males were subjected to a thorough history, sexual habit and clinical examination. A routine haemogram, Liver Function Test, Kidney Function Test, hormone profile and antisperm antibody titre was conducted. Seminal fluid examination was done within 2 hours of ejaculation at three different centres with a 3 days period of abstinence before each test.

All these 50 patients were then treated with daily dose of 8 mg of Lycopene (Lycored) till their sperm analysis showed optimal level [Table - 1] or pregnancy was achieved. Patients were regularly followed up with sperm analysis. Results was then analysed.

We present our result after a twelve months follow-up as follows:

Results

All 50 patients completed the trial with very good patients compliance and no adverse reaction noted in a 12 months follow-up.

Seminal fluid analysis showed improvement in sperm count in 35 patients (70%) and improvement in functional sperm concentration (FSC) in 30 patients (60%). Sperm motility improved to optimal level in 27 patients (54%) while sperm motility index (SMI) improved in 23 patients (46%), and improvement in sperm morphology was seen in 19 patients (38%) though much more was expected. [Table - 2]

In total in 18 patients (36%) all the parameter of sperm analysis showed improvement to optimal level [Table - 1] making them proud fathers. The pregnancy rate (36%) was mostly seen at the end of 3 months of therapy followed by end of 6 months of therapy and thereafter reduced. [Table - 3]

Discussion

Controlled generation of ROS has a physiological role in spermatozoal function such as hyperactivation. capacitation acrosome reaction[42],[14] but increased levels of ROS has been found in the semen of infertile males[15],[16] and this results in DNA fragmentation.[8] Defective sperm function is the most common cause of idiopathic male infertility and until recently it was difficult to evaluate and treat. This was partly due to our incomplete understanding of the factors constituting normal and abnormal sperm function leading to male infertility. The excessive generation of reactive oxygen species (ROS) by abnormal spermatozoa contaminated leukocytes (Leukocytospermia) has been identified as one of the few defined etiologies for idiopathic male infertility (Sikka SC 1996). Lycopene is present in high concentration in testis, prostate and adrenals. Epidemiological studies suggest that people living in the Mediterranean region who consume more tomatoes. watermelon and other fruits and vegetable rich in Lycopene have reduced risk of developing infertility (both males/females).

The result of these studies consider Lycopene as being responsible for these beneficial effects.

Recent data published show that Lycopene supplementation offer promise of increased sperm production as well as survival in idiopathic oligoasthenospermia.

Lycored, an extract from Lycopene rich tomatoes is 100% natural, commercially available Lycopene.

Genitourinary infection/inflammation, ageing and environmental toxicants create oxidative stress status resulting in oligoasthenospermia.

Lenzi Geva and Sulciman SA in their respective studies[9],[43],[44] have shown that idiopathic infertile males treated with Lycopene demonstrated improved semen characteristic. fertilisation in vitro and higher pregnancy rate.

In our study we found that maximum beneficial effect was observed in improvement of sperm count and functional sperm concentration followed by improvement in sperm motility percentage and sperm motility index. Though improvement in sperm morphology was observed much more was expected. No adverse effects were observed and patients compliance was good. A total pregnancy rate of 36% was observed in our study at the end of 12 month follow-up.

We attribute our good pregnancy rate of 36% due to use of high dose of lycopene (8 mg) once daily and meticulous screening of only those patients who had no other definite cause for their infertility with normal hormoneprofile and antisperm antibody titre.

Our study clearly justifies the role of Lycopene (Lycored) in management of idiopathic male infertility due to oligoasthenospermia but a long term study is desired to establish its credentials.

Conclusion

Lycopene (Lycored) supplementation improved sperm count, motility and morphology to optimum level in oligoasthenospermia infertile males, making them proud fathers.

References

1.	Sikka SC. Oxidative Stress and Role of Antioxidants in Normal and Abnormal Sperm Function. Front Biosci 1: 78-86.
2.	Alkan l, Simsek F, Haklar G et al. Reactive oxygen species production by the spermatozoa of patients with idiopathic infertility: Relationship to seminal plasma antioxidants. J Urol 1997: 157: 140-143.
3.	Sharma RK et al. Reactive oxygen species and male infertility. Urology 1996:48: 835-850.
4.	Aitken RJ et al. Differential contribution of leukocytes and spermatozoa to the generation of reactive oxygen species in the ejaculates of oligozoospermic patients and fertile donors. J Reprod Fertil 1992: 94: 451-462.
5.	Aitken RJ et al. Generation of reactive oxygen species, lipid peroxidation and human sperm function. Biol Reprod 1989: 40: 183-197.
6.	Lewis SE et al. Total antioxidant capacity of seminal plasma is different in fertile and infertile men. Fertile Steril 1995: 64: 868-870.
7.	Lewis SE et al. Total antioxidant capacity of seminal plasma is different in fertile and infertile men. Fertile Steril 1995: 64: 868-870.
8.	Oztez S et al. Invitro effects of peroxynitrite on human spermatozoa. Andrologia 1999: 31: 195-198.
9.	Irvine DS et al. DNA integrity in human spermatozoa: relationships with semen quality. J Androl 2000; 21: 33-34.
10.	Smith R et al. Total antioxidant capacity of human seminal plasma. Hum Reprod 1996: I I: 1655-1660.
11.	Aitken RJ et al. Prospective of sperm-oocyte fusion and ROS generation as a criteria for the diagnosis of infertility. Am J Obstet Gynecol 1991: 164: 542-551.
12.	Barbieri ER et al. Varicocele-associated decrease in antioxidant defences. J Androl 1999: 20: 713-717.
13.	Hendin BN et al. Varicocele is associated with elevated spermatozoal ROS production and diminished seminal plasma antioxidant capacity. J Urol 1999: 161: 1831-1834.
14.	Aitken RJ. Molecular mechanisms regulating sperm functions. Mol Hum Reprod 1997: 3: 169-173.
15.	De Lamirande E et al. Impact of reactive oxygen species on spermatozoa, a balancing act between beneficial and detrimental effects. Hum Reprod 1995: 10: 15-21.
16.	Alvarez JF et al. Spontaneous lipid peroxidation and production of hydrogen peroxide and superoxide in human spermatozoa. J Androl 1987: 8: 338-348.
17.	Lopes S et al. ROS: Potential cause for DNA fragmentation in human spermatozoa. Hum Reprod 1998: 13: 896-900.
18.	Fabio F et al. Relationship between oxidative stress, semen characteristics, and clinical diagnosis in men undergoing infertility investigation. Fertil Steril 2000; 73: 459-464.
19.	Jones et al. Peroxidative breakdown of Phospholipids in human spermatozoa, spermicidal properties of fatty acid peroxides and protective action of seminal plasma. Fertile Steril 1979: 31: 531-537.
20.	Aitken RJ, West et al. Analysis of the relationship between ROS production and leukocytes infiltration in fractions of human semen separated on percoll gradients. Int J Androl 1990; 13: 433-451.
21.	Man'kovs'ka IM et al. The role of oxygen radicals in the physiology and pathology of human sperm. Fiziol Zh 1998; 44: 118-125.
22.	Aitken RJ et al. Cellular basis of defective sperm function and its association with the genesis of ROS by human spermatozoa. J Reprod Fertile 1987: 81: 459-469.
23.	Aitken RJ et al. Analysis of relationship between defective sperm function and the generation of ROS in cases of oligozoospermia. J Androl 1989; 10: 214-220.
24.	Miesel R et al. Copper dependent defences in inflammatory and autoimmune rheumatic diseases. Inflammation 1993.
25.	Hughes CM et al. The effects of antioxidants supplementation during percoll preparation on human sperm DNA integrity. Hum Reprod 1998; 13: 1240-1247.
26.	Conte G et al. Reactive oxygen species in male infertility: Review of literature and personal observations. Panminerva Med 1999; 41: 45-53.
27.	Lenzi A et al. Placebo controlled, double blind. cross over trial of glutathione therapy in male infertility. Hum Reprod 1993; 10: 1657-1662.
28.	Ochsendorf FR. Infections in the male genital tract and ROS. Hum Reprod Update 1999: 5: 399-420.
29.	Rao B et al. Lipid peroxidation in human spermatozoa as related to midpiece abnormalities and motility. Gamete Research 1989; 24: 127-134.
30.	Selley ML et al. Content of significant amounts of cytotoxic end products of lipid peroxidation in human semen. J Reprod Fertile 1991: 92: 291-298.
31.	Stahl W et al. Cis-trans isomers of lycopene and beta carotene in human serum and tissues. Arch Biochem Biophys 1991294: 173-177.
32.	Palan P, Naz R. Changes in various antioxidant levels in human seminal plasma related to immunoinfertility. Arch Androl 1996: 36: 139-143.
33.	Hughes CM et al. The effects of antioxidant supplementation during Percoll preparation on human sperm DNA integrity. Hum Reprod 1998; 13: 1240-1247.
34.	Di Mascio P, Kaiser S. Sies H. Lycopene as the most efficient biological carotenoid singlet oxygen quencher. Arch Biochem Biophys 1989: 274: 532-538.
35.	Griveau JF, de Lannou D. Reactive oxygen species and human spermatozoa. Int J Androl 1997; 20: 61-69.
36.	Lenzi A, Culasso F. Gandini L, Lombardo F, Dondero F. Placebo controlled, double blind, cross over trial of glutathione therapy in male infertility. Hum Reprod 1993: 10: 1657-1662.
37.	Geva E. Bartoov B. Zabludovski N et al. The effect of antioxidant treatment on human spermatozoa and fertilization rate in an in vitro fertilization program. Fertil Steril 1996: 66: 430-434.
38.	Suleiman SA et al. Lipid peroxidation and human sperm motility: protective role of vitamin E. J Androl 1996; 17: 530-537.
39.	Wang Y, Aggrawal A et al. Importance of reactive oxygen species in the peritoneal fluid of women with endometriosis or idiopathic infertility. Fertil Steril 1997; 68: 826-830.
40.	Di Mascio P, Kaiser S. Sies H. Lycopene as the most efficient biological cartenoid singlet oxygen quencher. Arch Biochem Biophys 1989; 274: 532-538
41.	Helga Erster MA et al. The potential role of Lycopene for human health. J Am Coll Nutr 1997.
42.	Lewis EM et al. Comparison of individual antioxidants of sperm and seminal plasma in fertile and infertile men. Fertil Steril 1997: 67: 142-147.
43.	Shen H et al. Detection of oxidative DNA damage in human sperm and its association with sperm function and male infertility. Free Radic Biol Med 2000; 28: 529-536.
44.	Sun JG et al. Detection of DNA fragmentation in human sperm: correlation with fertilization in vitro. Biol Reprod 56: 602-607.