We explain environmental and genetic factors determining male genetic conditions and infertility and evaluate the significance of environmental stressors in shaping defensive responses, which is used in the diagnosis and treatment of male infertility. This is done through the impact of external and internal stressors and their instability on sperm parameters and their contribution to immunogenetic disorders and hazardous DNA mutations. As chemical compounds and physical factors play an important role in the induction of immunogenetic disorders and affect the activity of enzymatic and non-enzymatic responses, causing oxidative stress, and leading to apoptosis, they downgrade semen quality. These factors are closely connected with male reproductive potential since genetic polymorphisms and mutations in chromosomes 7, X, and Y critically impact on spermatogenesis. Microdeletions in the Azoospermic Factor AZF region directly cause defective sperm production. Among mutations in chromosome 7, impairments in the cystic fibrosis transmembrane conductance regulator CFTR gene are destructive for fertility in cystic fibrosis, when spermatic ducts undergo complete obstruction. This problem was not previously analyzed in such a form. Alongside karyotype abnormalities AZF microdeletions are the reason of spermatogenic failure. Amongst AZF genes, the deleted in azoospermia DAZ gene family is reported as most frequently deleted AZF. Screening of AZF microdeletions is useful in explaining idiopathic cases of male infertility as well as in genetic consulting prior to assisted reproduction. Based on the current state of research we answer the following questions: (1) How do environmental stressors lessen the quality of sperm and reduce male fertility; (2) which chemical elements induce oxidative stress and immunogenetic changes in the male reproductive system; (3) how do polymorphisms correlate with changes in reproductive potential and pro-antioxidative mechanisms as markers of pathophysiological disturbances of the male reproductive condition; (4) how do environmental stressors of immunogenetic disorders accompany male infertility and responses; and (5) what is the distribution and prevalence of environmental and genetic risk factors.

Between 1998 and 2001 the last remaining wild grey partridge (Perdix perdix) population in Ireland faced imminent extinction with an estimated spring population of 4–6 pairs, and an autumn population of 22–24 birds. A captive breeding programme began in 2002 with two pairs of grey partridge. In the most successful year in 2010, 39 pairs produced a total of 510 chicks. Average chick survival rate was 65.13%. At 88.9 the highest chick survival rate was achieved in 2011. Chick survival of parent–reared birds in captivity is defined by the number of juveniles surviving at age six weeks: similar to estimations used for wild populations of grey partridge. Family coveys were released in late summer to early autumn. In most instances the entire family cohort was released as one unit. However, in coveys of twenty or above, an average of five parent–reared poults were held back as breeding stock for the following year. In early spring of the following year, birds held back were paired with single males or females trapped from the wild. The techniques we used were traditional and labour intensive but highly effective. We recommend that other grey partridge recovery projects should consider captive breeding using the methods employed in this programme to compliment other game management methods used.

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This review assessed relationships between external factors and the level of joint pathology (hip, knee, ankle, elbow, shoulder, hands and feet) in humans with dysplastic arthritis, psoriatic arthritis, rheumatoid arthritis, Sjögren's syndrome, systemic lupus erythematosus, systemic sclerosis, degenerative joint disease, ankylosing spondylitis, osteoporosis, osteomalacia and gout. The accumulation of physiologically different chemical elements in different types of bones in humans of different ages allows for a more accurate assessment of the causal quoted response from parallel biochemical systems. These allow a better understanding of the link between exposure arising from smoking, alcohol, drugs, diseases, heredity, effects of amalgam dental fillings, diet, food preferences, chemical elements, occupational and environmental exposure to toxicants, lipoperoxidation and pro-antioxidant reactions. Physiology of the osteoarticular system determines what is responsible for bone and long-term body accumulation of toxic metals, which may be involved in the pathogenesis of bone diseases. While relationships between stressors, antioxidant system and bone condition predict potential risks in certain abnormalities and change oxidative stress. Elemental instability in the environment combined with salinity, acidity, redox potential and local changes in hydrochemical balance, enhances adverse effects. Processes of remodeling and bone mineralization continue throughout life and therefore may be a determinant of long-term accumulation of toxicants. Environmental issues affecting bioaccumulation of chemical elements in the osteoarticular system in humans is poorly understood. Alloplastic procedures, including the need for prostheses, supplemented by image layouts oxidative enzyme activities, as well as lipoperoxidation and the level of stress proteins, give a complete picture of skeletal response to external stressors. Simultaneously, the analysis of the impact of stressors on bones allows a more accurate tracing of causal quoted responses from parallel reactions. They have a direct relationship with stressors and affect the nature and degree of responses and defense capabilities. Thus they have a role in the diagnosis of diseases of the skeletal system.