Zinc
Zinc deficiency in humans will increase susceptibility to infectious diseases. Zinc is also important for host immunity. Mild zinc deficiency can impair multiple mediators of host immunity, ranging from the physical barrier on the skin to acquired cellular and humoral immunity. ( Frost el al ., 1977 ; Oleske et al ., 1979 ; Good ,1981 ; Walsh et al ., 1994)
Zinc deficiency
Zinc intake is in the range 8-12 mg /day. Marginal zinc deficiency (intake > 5mg/day) will have clinical signs such as depressed immunity , impaired taste and smell ,onset of night blindness , impairment of memory and decrease in spermatogenesis in males ( Prasad et al ., 1961 ; Standstead et al ., 2000)Serve zinc deficiency will lead to severely depressed immune function ,frequent infections , bullous pustular dermatitis , diarrhoea , aplopecia and mental disturbance. (Barnes and Moynahan 1973)
Zinc and the cell cycle
Zinc is required during the mid to late GI phase of the cell cycle in promotion of thymidine kinase expression(Chester et al., 1993)and in another less well-defined step involved in cell transition to S phase. Activated lymphocytes take up zinc via multiple mechanisms, including receptors for zinc transferring ,metallothionein, albumin and α₂-macroglobulin (Walsh et al ., 1994 ; Shankar and Prasad , 1998 ; Prasad , 2000a)and also by other less well- characterized mechanism , such as anionic channels or transporters.A greater proportion of S-compared with G2-phase cells was observed among mitogen-stimulated lymphocytes from mildly zinc deficient patients syffering from sickle-cell anaemia(Prasad 2000a).
Zinc and cell replication
Zinc influences the activity of multiple enzymes which act at the very basic levels of replication and transcription. (Walsh et al ., 1994 ; Zalewki , 1996 ; Shankar and Prasad ,1998)Zinc forms the active enzymetic sites of many metalloproteases. The activity of the major enzyme regulating DNA replication, DNA polymerase, is zinc dependent. It is inhibited by zinc deficiency and zinc chelators and is enhanced by addition of low concentration s of idines , is also very sensitive to dietary zinc depletion.
Zinc and lymphocyte activation
Zinc plays a role in multiple aspects of T lymphocyte activation and signal transduction. Zinc has implication with tyrosine, an essential protein in the early step of T- cell activation.(Turner et al., 1990) Zinc stimulates autophosphorylation of tyrosine residues by tyrosine kinase and subsequent phosphorylation of the T-cell-receptor complex . (Zalewki, 1996)Zinc affects the phosphorylation of proteins that regulate activation and cell proliferation.
Zinc in antioxidant defence
Zinc protect cells from the damaging effect of oxygen radicals such as superoxide during immune activation. (Taylor and Bray ,1991)
Effects of zinc deficiency on barrier function
Zinc deficiency damages epidermal cells, resulting in skin lesions. (Shankar and Prasad, 1998)
Effects on zinc on immune-cell numbers
Zinc deficiency will lead to lymphopenia that occurs in both the central and peripheral lymphoid tissue. (Walsh et al., 1994) B-cell that develops in the bone marrow is adversely affected by zinc deficiency (Walsh et al., 1994 Shankar and Prasad, 1998)
Neutrophil functions
Neutrophil chemotaxis and functions are impaired in zinc deficiency (Walsh et al., 1994 Shankar and Prasad, 1998)Zinc improved the meutrophil response against Staphylococcus . (Singh et al ., 1994)
Monocyte functions
Chemotatic responses of monocytes are suppressed during zinc deficiency. (Walsh et al., 1994 Shankar and Prasad, 1998) Monocytes are impaired in killing of intracellur parasites and reduced in macrophage phagocytosis. (Schlesinger et al., 1993)
Natural killer cell function
Zinc deficiency caused a decrease in natural killer cells activity . (Walsh et al., 1994 Shankar and Prasad, 1998) Zinc mediated inhibition of natural killer cells activity decrease is due to natural killer cells inhibitory receptor requires zinc.( Rajagopalan et al ., 1995)
T and B-cell functions
B- cell proliferative and antibody responses are inhibited by zinc deficiency ( Moulder and Steward , 1989 ; Walsh et al ., 1994 ; Shankar and Prasad , 1998)T- dependent antibody responses are more affected by zinc deficiency than T-independent ones (Franker et al ., 1977 ,1978 ,1984 ,1986)
Effect on high doses of zinc
Very high zinc intake in adults and children can result in copper deficiency and this could cause immunosupression (Porter et al ., 1977 ; Prasad et al ., 1978 ; Fosmire , 1990)
The influence of zinc on conditions involving immunosupression
Patients suffering from sickle cell disease have depressed peripheral T-cell numbers ,and decreased natural killer cell activity .( Prasad ,200a) For patients with Down’s syndrome , zinc supplements can restore immediate hypersensitivity , lymphocyte functions and neutrophil chemotaxis and increase resistance to infection (Bjorksten et al ., 1980)
Zinc deficiency in humans will increase susceptibility to infectious diseases. Zinc is also important for host immunity. Mild zinc deficiency can impair multiple mediators of host immunity, ranging from the physical barrier on the skin to acquired cellular and humoral immunity. ( Frost el al ., 1977 ; Oleske et al ., 1979 ; Good ,1981 ; Walsh et al ., 1994)
Zinc deficiency
Zinc intake is in the range 8-12 mg /day. Marginal zinc deficiency (intake > 5mg/day) will have clinical signs such as depressed immunity , impaired taste and smell ,onset of night blindness , impairment of memory and decrease in spermatogenesis in males ( Prasad et al ., 1961 ; Standstead et al ., 2000)Serve zinc deficiency will lead to severely depressed immune function ,frequent infections , bullous pustular dermatitis , diarrhoea , aplopecia and mental disturbance. (Barnes and Moynahan 1973)
Zinc and the cell cycle
Zinc is required during the mid to late GI phase of the cell cycle in promotion of thymidine kinase expression(Chester et al., 1993)and in another less well-defined step involved in cell transition to S phase. Activated lymphocytes take up zinc via multiple mechanisms, including receptors for zinc transferring ,metallothionein, albumin and α₂-macroglobulin (Walsh et al ., 1994 ; Shankar and Prasad , 1998 ; Prasad , 2000a)and also by other less well- characterized mechanism , such as anionic channels or transporters.A greater proportion of S-compared with G2-phase cells was observed among mitogen-stimulated lymphocytes from mildly zinc deficient patients syffering from sickle-cell anaemia(Prasad 2000a).
Zinc and cell replication
Zinc influences the activity of multiple enzymes which act at the very basic levels of replication and transcription. (Walsh et al ., 1994 ; Zalewki , 1996 ; Shankar and Prasad ,1998)Zinc forms the active enzymetic sites of many metalloproteases. The activity of the major enzyme regulating DNA replication, DNA polymerase, is zinc dependent. It is inhibited by zinc deficiency and zinc chelators and is enhanced by addition of low concentration s of idines , is also very sensitive to dietary zinc depletion.
Zinc and lymphocyte activation
Zinc plays a role in multiple aspects of T lymphocyte activation and signal transduction. Zinc has implication with tyrosine, an essential protein in the early step of T- cell activation.(Turner et al., 1990) Zinc stimulates autophosphorylation of tyrosine residues by tyrosine kinase and subsequent phosphorylation of the T-cell-receptor complex . (Zalewki, 1996)Zinc affects the phosphorylation of proteins that regulate activation and cell proliferation.
Zinc in antioxidant defence
Zinc protect cells from the damaging effect of oxygen radicals such as superoxide during immune activation. (Taylor and Bray ,1991)
Effects of zinc deficiency on barrier function
Zinc deficiency damages epidermal cells, resulting in skin lesions. (Shankar and Prasad, 1998)
Effects on zinc on immune-cell numbers
Zinc deficiency will lead to lymphopenia that occurs in both the central and peripheral lymphoid tissue. (Walsh et al., 1994) B-cell that develops in the bone marrow is adversely affected by zinc deficiency (Walsh et al., 1994 Shankar and Prasad, 1998)
Neutrophil functions
Neutrophil chemotaxis and functions are impaired in zinc deficiency (Walsh et al., 1994 Shankar and Prasad, 1998)Zinc improved the meutrophil response against Staphylococcus . (Singh et al ., 1994)
Monocyte functions
Chemotatic responses of monocytes are suppressed during zinc deficiency. (Walsh et al., 1994 Shankar and Prasad, 1998) Monocytes are impaired in killing of intracellur parasites and reduced in macrophage phagocytosis. (Schlesinger et al., 1993)
Natural killer cell function
Zinc deficiency caused a decrease in natural killer cells activity . (Walsh et al., 1994 Shankar and Prasad, 1998) Zinc mediated inhibition of natural killer cells activity decrease is due to natural killer cells inhibitory receptor requires zinc.( Rajagopalan et al ., 1995)
T and B-cell functions
B- cell proliferative and antibody responses are inhibited by zinc deficiency ( Moulder and Steward , 1989 ; Walsh et al ., 1994 ; Shankar and Prasad , 1998)T- dependent antibody responses are more affected by zinc deficiency than T-independent ones (Franker et al ., 1977 ,1978 ,1984 ,1986)
Effect on high doses of zinc
Very high zinc intake in adults and children can result in copper deficiency and this could cause immunosupression (Porter et al ., 1977 ; Prasad et al ., 1978 ; Fosmire , 1990)
The influence of zinc on conditions involving immunosupression
Patients suffering from sickle cell disease have depressed peripheral T-cell numbers ,and decreased natural killer cell activity .( Prasad ,200a) For patients with Down’s syndrome , zinc supplements can restore immediate hypersensitivity , lymphocyte functions and neutrophil chemotaxis and increase resistance to infection (Bjorksten et al ., 1980)
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