title: Role of Oxidative Stress in Male Reproductive Dysfunctions with Reference to Phthalate Compounds.
abstract: OBJECTIVE
  A wide variety of environmental chemicals/xenobiotics including phthalates have been shown to cause oxidative stress targeting the endocrine system and cause reproductive anomalies. The present review describes various issues by oxidative stress causing male reproductive dysfunctions. Here in this review, the importance and role of phthalate compounds in male reproductive dysfunction has been well documented.
  
  
  METHODS
  One class of environmental endocrine disruptors is phthalates. Phthalate compounds are mostly used as plasticizers, which increase the flexibility, durability, longevity, and etc. of the plastics. Large-scale use of plastic products in our daily life as well as thousands of workers engaged in the manufacture of plastic and plastic products and recycling plastic industry are potentially exposed to these chemicals. Further, general population as well as vulnerable groups i.e. children and pregnant women are also exposed to these chemicals. Phthalates are among wide variety of environmental toxicants capable of compromising male fertility by inducing a state of oxidative stress in the testes. They may also generate reactive oxygen species (ROS) that may affect various physiological and reproductive functions.
  
  
  RESULTS
  The available data points out that phthalate compounds may also induce oxidative stress in the male reproductive organs mainly testis and epididymis. They impair spermatogenic process by inducing oxidative stress and apoptosis in germ cells or target sertoli cells and thereby hamper spermatogenesis. They also impair the Leydig cell function by inducing ROS, thereby decreasing the levels of steroidogenic enzymes.
  
  
  CONCLUSIONS
  Thus in utero and postnatal exposure to phthalate compounds might lead to decreased sperm count and various other reproductive anomalies in the young male.
authors.affiliation: Reproductive and Cytotoxicology Department, National Institute of Occupational Health (ICMR), Meghani Nagar, Ahmedabad-380016, Gujarat, India. s.microb@yahoo.com.
authors.forename: Sapna
authors.initials: S
authors.lastname: Sedha
authors.affiliation: Reproductive and Cytotoxicology Department, National Institute of Occupational Health (ICMR), Meghani Nagar, Ahmedabad-380016, Gujarat, India.
authors.forename: Sunil
authors.initials: S
authors.lastname: Kumar
authors.affiliation: Department of Food Science and Technology, Yeungnam University, 280 Daehak-ro, Gyeongsan-si, Gyeongsangbuk-do 712-749, Republic of Korea.
authors.forename: Shruti
authors.initials: S
authors.lastname: Shukla
mesh_terms: D004249:DNA Damage / Q000187:drug effects; D052244:Endocrine Disruptors / Q000378:metabolism / Q000633:toxicity*; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D006059:Gonadal Dysgenesis / Q000139:chemically induced*; D006801:Humans; D007248:Infertility, Male / Q000139:chemically induced; D007985:Leydig Cells / Q000187:drug effects; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010795:Phthalic Acids / Q000378:metabolism / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced*; D012098:Reproduction / Q000187:drug effects*; D013076:Sperm Count; D013091:Spermatogenesis / Q000187:drug effects; D013737:Testis / Q000002:abnormalities*
chemical_list: D052244:Endocrine Disruptors; D010795:Phthalic Acids