Male sterility

Male infertility
Falling average sperm count
Drop in sperm vitality
Inadequate sperm quality
Pollution and male fertility
Declining sperm counts
Impaired male fertility

Cytoplasmic male sterility is total or partial male sterility in hermaphrodite organisms, as the result of specific nuclear and mitochondrial interactions. Male sterility is the failure to produce functional anthers, pollen, or male gametes. Such male sterility in hermaphrodite populations leads to gynodioecious populations (populations with coexisting fully functioning hermaphrodites and male-sterile hermaphrodites).

Cytoplasmic male sterility, as the name indicates, is under extranuclear genetic control (under control of the mitochondrial or plastid genomes). It shows non-Mendelian inheritance, with male sterility inherited maternally. In general, there are two types of cytoplasm: N (normal) and aberrant S (sterile) cytoplasms. These types exhibit reciprocal differences.

Source: Wikipedia

Sperm are manufactured over 75 days and are susceptible throughout that period to chemical exposure. The variation within a single man is huge: from 7 million/ml to 170 million/ml. It was generalized that the concentration of sperm in semen of men in Denmark has dropped from an average of 113 million per ml in 1940 to around 66 million in 1993. Seminal volume dropped from 3.40 ml in 1940 to 2.75 ml in 1990. One reason may be a reduction in the number of Sertoli cells, also known as nurse cells, which are responsible for orchestrating and controlling the process of sperm production. The number of Sertoli cells is determined at the foetal, or neonatal, stage in human development. Once this is fixed it places an absolute upper limit on the number of sperm that a man can manufacture in a given time. The growth of male testes and the multiplication of Sertoli cells is catalyzed by follicle stimulating hormone (FSH). The unrestrained action of FSH alone would lead eventually to the creation of enormous testes and so oestrogen is used in a "negative feedback loop" to control the supply of FSH. If there is excess oestrogen floating around at the time of Sertoli cell multiplication, it can cut off the supply of FSH before it has a chance to get to work< The development of an embryo's testes occurs between weeks six and twenty of pregnancy, when the levels of female hormone are at their lowest. Anyway, these natural oestrogens cannot interfere with the foetus. However, any other female hormones - or chemicals that mimic their effects - at this time could disrupt normal development. More than 30 manmade chemicals in the environment are known to have such oestrogenic properties and can be absorbed into the bloodstream though the gut. They include the aromatic hydrocarbons in car exhausts, PCBs (polychlorinated biphenyls) and DDT. In addition, modern cows lactate even when pregnant and the milk produced at these times is rich is oestrogens and passed on to the consumer without comment. The theory that the build up of manmade chemicals in the environment - many of which mimic female hormones - is causing male infertility has lead to an approach that measures the decrease in fertility based upon the year of birth.
Among the factors that can cause male infertility are semen disorders, systemic disease, genital infection, genetic defects, and drugs. Also cocktails of pesticides and other chemicals in the environment are believed to be affecting male foetuses by blocking testosterone in the womb or imitating oestrogen, so disrupting male sexual development and function.
Over the same period of decreasing male fertility there has been a growth in testicular cancer and other genital abnormalities such as cryptorchidism (undescended testicles in children) and hypospadias. Testicular cancer is correlated with severely depressed semen quality.

Such remarkable changes in semen quality and the occurrence of genitourinary abnormalities may have a common cause.

(D) Detailed problems