Mammals thyroid hormones

Atrophy of the thymus is a consistent finding in mammals poisoned by 2,3,7,8-TCDD, and suppression of thymus-dependent cellular immunity, particularly in young animals, may contribute to their death. Although the mechanisms of 2,3,7,8-TCDD toxicity are unclear, research areas include the role of thyroid hormones (Rozman et al. 1984) interference with plasma membrane functions (Matsumura 1983) alterations in ligand receptors (Vickers et al. 1985) the causes of hypophagia (reduced desire for food) and subsequent attempts to alter or reverse the pattern of weight loss (Courtney et al. 1978 Seefeld et al. 1984 Seefeld and Peterson 1984) and excretion kinetics of biotransformed metabolites (Koshakji et al. 1984). 

Such observations as these should inject caution into those who speak glibly about what metabolism is like in the mammalian organism. Furthermore, if differences such as these exist among different species of higher mammals, it lends credence to the idea that, within the human species, quantitative differences of a similar nature may exist. Because of differences in enzyme systems and the extent to which different metabolic pathways are utilized in different individuals, it is not at all unreasonable to conclude that different individuals probably have fundamental needs for quite different levels of the thyroid hormone. 

Mammals have several classes of hormones, distinguishable by their chemical structures and their modes of action (Table 23-1). Peptide, amine, and eicosanoid hormones act from outside the target cell via surface receptors. Steroid, vitamin D, retinoid, and thyroid hormones enter the cell and act through nuclear receptors. Nitric oxide also enters the cell, but activates a cytosolic enzyme, guanylyl cyclase (see Fig. 12-10). 

Thyroxine and triiodothyronine have many effects, a major one in mammals and birds being stimulation of energy metabolism in tissues. It has long been recognized that a deficiency of thyroid hormone is reflected in an overall lower basal metabolic rate (Chapter 6). Maley and Lardy observed that thyroxine uncouples oxidative phosphorylation (Chapter 18) in isolated mitochondria.117 When mitochondria from animals receiving extra thyroxine were compared with those from control animals, an increased rate of electron transport was observed. However, there was little or no change in the P / O ratio. Thus, the hormone apparently increased the rate of electron transport... 

There is no such clear cut difTcrcnlialiun as metamorphosis in the mammal, but development is an extremely complex process and has been shown to depend upon the presence of adequate amounts of thyroid hormones. Deficient development, especially of the central nervous system, is marked in ehildren suffering from thyroid deficiency early in life, ansi this inadequacy cannot be overcome completely by medication commenced after the first few weeks. In the adult, thyroxine is important in the maintenance of energy turnover in most of the tissues of the body, such as the heart, skeletal muscle, liver, and kidney, Other physiological functions, most notably brain aclivity and reproduction, are also dependent upon thyroxine, although the metabolic rales of the tissues concerned in these functions do not seem to be altered. 

Seals and Other Marine Mammals. Among the effects of CACs reported on free-ranging seals are skeletal deformities and impaired reproduction. Captive seals fed with CAC contaminated hsh showed a significantly reduced reproductive success compared to animals fed with clean hsh.93 Vitamin A and thyroid hormone levels were also signihcantly reduced.89 These hndings corresponded to results of experimental studies with mink and rodents exposed to PCBs. 

In contrast to arsenic, trace concentrations of selenium are essential for human and animal health. Until the late 1980s, the only known metabolic role for selenium in mammals was as a component of the enzyme glutathione peroxidase (GSH-Px), an anti-oxidant that prevents cell degeneration. There is now growing evidence, however, that a seleno-enzyme is involved in the synthesis of thyroid hormones (Arthur and Beckett, 1989 G. F. Combs and S. B. Combs, 1986). Selenium dehciency has been linked to cancer, AIDS, heart disease, muscular dystrophy, multiple sclerosis, osteoarthropathy, immune system and reproductive disorders in humans, and white muscle disease in animals (Levander,... 

Figure 11-11 depicts the several structures relevant to this discussion. The thyroid hormones and precursors are all iodinated tyrosine derivatives, and their iodine content is undoubtedly a unique occurrence in mammals. 

Iodine is an essential element in humans and other mammals, which is used for the synthesis of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). These hormones play a prominent role in the metabolism of most cells of the organism and in the process of early growth and development of most organs, especially brain (Anderson et al., 2000). Besides T3 and T4, reverse T3 (rT3), monoiodotyrosine (MIT), and diiodotyrosine (DIT) are also synthesized and distributed in the body of humans and animals, but only T3 and T4 have a biological function. Iodine in the human body mainly comes through dietary and water intake, and inhalation of atmospheric iodine. Due to low concentrations of iodine in the air (10—20ng/m ), food and water intake form the major source of iodine for adults, while for infants it is milk. The concentration of iodine in foodstuffs is directly related to that in the environment where the foods come from. Iodine deficiency disorders are mainly found in places where the concentration of iodine in the soil and drinking water is very low. In the water, foodsmffs, and... 

In the human and mammal body, iodine exists as thyroid hormones T4 and T3, as well as MIT, DIT and rT3, which are mainly bound with proteins in thyroid and other tissues. 

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