Sulfur deficiency symptom

Adults who lack protein may feel dizzy and nauseated.Their skin becomes dry and scaly, they fatigue easily, and they become short-tempered. Infections, kidney problems, and diarrhea become increasingly worse. Since protein is the main source of sulfur intake, both kwashiorkor and marasmus produce sulfur deficiency symptoms. 

Plants deficient in sulfur are smaller than normally developed plants. If the deficiency occurs at an earlier stage, the plants are stunted and have a rigid, erect appearance. Some sulfur-deficiency symptoms observed in, for example, the Dark Yellow Fuji Mefo chrysanthemum, included branchless roots that aged earlier, shorter stems, smaller leaves and overall yellowing of new leaves. Without sulfur, plants did not produce flowers suitable for commercial sale (Huang et al. 1997). 

While defects in protein XPD often cause typical XP symptoms, some defects in the same protein lead to trichothiodystrophy (TTD, brittle hair disease). The hair is sulfur deficient, and scaly skin (ichthyosis, Box 8-F), mental retardation, and other symptoms are observed.0 Like their yeast counterparts (proteins RAD3 and RAD25), XPB and XPD are both DNA helicases.0 They also constitute distinct subunits of the human transcription factor TFIIHP, which is discussed in Chapter 28. It seems likely that XPD is involved in transcription-coupled repair (TCR) of DNA.° °i-s This is a subpathway of the nucleotide excision repair (NER) pathway, which allows for rapid repair of the transcribed strand of DNA. This is important in tissues such as skin, where the global NER process may be too slow to keep up with the need for rapid protein synthesis. Transcription-coupled repair also appears to depend upon proteins CSA and CSB, defects which may result in the rare cockayne syndrome.13 0 4 11 Patients are not only photosensitive but have severe mental and physical retardation including skeletal defects and a wizened appearance. 

A complete diet must supply the elements carbon, hydrogen, oxygen, nitrogen, phosphorus, sulfur, and at least 18 other inorganic elements. The major elements are supplied in carbohydrates, lipids, and protein. In addition, at least 17 vitamins and water are necessary. If an essential nutrient is omitted from the diet, certain deficiency symptoms appear. 

The extent of the adverse effect of high sulfur intake in the diet of animals depends on species, the source of sulfur, and the concentration in feedstuffs. After depletion of the copper storages of the body, a sulfur exposure causes a secondary copper deficiency, especially in ruminants. In practice, it is difficult to distinguish between direct sulfur-induced toxic effects and secondary copper deficiency symptoms. 

Mineral deficiency strongly affects the development of leaves and of the photosynthetic apparatus. We were interested to know whether carbon flux is more restricted in mineral deficient leaves by the thylakoid system or the Calvin cycle. Spinach was grown under mineral deficiency as shown in Tab. 1. Leaves of different age were detached and photosynthesis and F was measured. Rates of photosynthesis were on a unit leaf area basis consistently higher in the control leaves than in leaves deficient in phosphorus, sulfur or nitrogen. Sulfur and old nitrogen deficient leaves were chlorotic. F was increased under all deficiency conditions and particularly so in old leaves of phosphate and nitrogen starved plants and in young leaves of sulfur-deprived plants. The increase in F clearly correlated with the development of pronounced deficiency symptoms and reduced rates of photosynthesis. The data indicate that mineral deficiency introduces flux limitations in the Calvin cycle. 

DEFICIENCY SYMPTOMS. Sulfur deficiencies are manifested primarily in retarded growth because of sulfur s association with protein synthesis. 

Deficiency or Toxicity in Humans. Molybdenum deficiency in humans results in deranged metaboHsm of sulfur and purines and symptoms of mental disturbances (130). Toxic levels produce elevated uric acid in blood, gout, anemia, and growth depression. Faulty utiH2ation results in sulfite oxidase deficiency, a lethal inborn error. 

A nutritional molybdenum deficiency with clinical symptoms similar to those of sulfite oxidase deficiency was identified in a human patient receiving long-term total parenteral nutrition (TPN) (Abumurad et al. 1981). The clinical symptoms included irritability leading to coma, tachycardia, tachypnea, and night blindness. A reduced intake of protein and sulfur-amino acids alleviated the symptoms, but they were aggravated by infusion of sulfite. The biochemical findings were low tissue sulfite oxidase activity a 25-fold increase in thiosulfate excretion a 70% reduction in urinary output of sulfate and a marked rise in plasma methionine. The clinical symptoms of molybdenum deficiency were totally eliminated by daily supplementation of 300 pg of the element. 

Carbohydrates, proteins, fats, and nucleic acids are composed of six elements carbon, hydrogen, nitrogen, oxygen, phosphorus, and sulfur. In addition to these, many other minerals are required for experimental mammals, and presumed to be required for humans. These are divided into two groups, bulk and trace elements, and are found in Table 23-7. Table 23-8 lists some elements whose functions are known, or whose deficiencies result in well-recognized symptoms. 

Molybdenum is considered an ultra-trace element with an approximate amount of 5 mg in the adult human body. It is a cofactor for at least three enzymes in humans (sulfite oxidase, xanthine oxidase, and aldehyde oxidase) and is involved in the catabolism of sulfur-containing amino acids, purine, and pyrimidine. A better understanding of human molybdenum metabolism is needed in order to give evidence-based recommendations regarding optimal nutrition, although molybdenum deficiency and associated pathological symptoms have not yet been observed in humans [74]. 

Thiamine Pyrophosphate is the coenzyme responsible for transferring active acetaldehyde and active glycolaldehyde. Simultaneously, it acts as co-decarboxylase, i.e. as the coenzyme for a lyase. The characteristic component is thiamine (vitamin Bi), one of the vitamins whose biologic role has been known longest the symptoms of thiamine deficiency (beriberi in man polyneuritis in animals) comprised one of the starting points in the study of vitamins. The name thiamine refers to its sulfur content. 

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