Some Selenium Responses in the Rat not Related to Vitamin E

McCoy, Kim E.; Weswig, P. H.

doi:10.1093/jn/98.4.383

Cited by 167 publications

(33 citation statements)

References 12 publications

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“…Selenium is an essential trace element in h,am;ms, animals and for the growth of ¢,¢11s in culture [1,2], Despite its known role in glutathione peroxidase [2,] . 'rod other selenoproteins [5], the mechanism of action o1" selenium in regulating cell growth remains to be eluci.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of epidermal growth factor (EGF) and insulin‐stimulated tyrosine phosphorylation of endogenous substrates by sodium selenate

Pillay¹,

Makgoba²

1992

FEBS Letters

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,Sodium selenatc stimulated tyrosin¢ g.hosphorylation o[. the epidermal i~rowth factor (EGF3 r¢cepior in A431 cells and enhanced the lyres=no phosphorylation of endogenous proteins in r~pons¢ to EGF in A431 cells and insulin in NIH 3'!"3 HIR3,S calls, Th¢~ effect== occurred without lhanlp=`: in lilland binding, ~:r¢ not abolished by mere=pie=thane: in the case o1" the EGF receptor, and appeared distinct from tile effects of vanadate, Th¢"~ r~ult`: support a role ['or selenium or selenoprot¢ins in re~uhttin= EGF ~nd insulin receptor tyrofin¢ kinas¢ activity and SUllitest a mechanism whereby selenium.contain=nil compounds eOlttribat¢ to c¢11 i~rowth.

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Section: Discussionmentioning

confidence: 99%

Enhancement of epidermal growth factor (EGF) and insulin‐stimulated tyrosine phosphorylation of endogenous substrates by sodium selenate

Pillay¹,

Makgoba²

1992

FEBS Letters

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“…They are important parts of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) as well as transport protein with antioxidant properties, ceruloplasmin (Crl) (a copperbinding protein), providing protection against peroxidative superoxide radicals damage. Through enzymatic or indirect action, they block destructive alteration of lipids, proteins, and nucleic acids by oxygen-derived free radicals, radiation, certain heavy metals, and other toxic substances (12). Vitamin E and GSH-Px have similar and complementary physiological roles in protecting cells from damage caused by endogenous peroxides (13).…”

Section: Introductionmentioning

confidence: 99%

Trace Elements and Electrolytes Homeostasis and Their Relation to Antioxidant Enzyme Activity in Brain Hyperexcitability of Epileptic Patients

Hamed

Abdellah

2004

J Pharmacol Sci

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Abstract. Epileptogenesis is a big challenge. Various experimental and human studies suggested that the homeostasis of trace elements, electrolytes, membrane lipid peroxidation, and antioxidants is crucial for brain function, and they were directly or indirectly implicated as taking part in the pathophysiology of neuronal excitability, neuronal excitotoxicity, and seizure recurrence and its resistance to treatment with antiepileptic drugs (AEDs). In addition, AEDs can also alter the homeostasis of trace elements, electrolytes, and seriously increase membrane lipid peroxidation at the expense of protective antioxidants, leading to an increase in seizure recurrence and an idiosyncratic drug effect. Differential effects were detected among different AEDs treatments in which carbamazepine (CBZ) was found to be better anticonvulsant for the control of free radical related seizures and the level of trace elements were better regulated with CBZ than with valproate (VPA) and phenytoin (PHT) therapies. It is concluded that adequate trace elements and antioxidants supply is important for brain functions and prevention of neurological diseases and further elucidation of the pathological actions of such substances in the brain should result in new therapeutic approaches. Trace elements and antioxidant might have neuroprotective biological targeted benefits when used in epileptic patients.

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“…Early light microscopic studies established that epididymal spermatozoa of selenium-deficient animals exhibit a reduction or loss of motility and display flagellar defects localized primarily to the midpiece. The abnormalities include both hairpin-like bends of the flagellum as well as breaks and/or separation of its axial fibers (McCoy & Weswig 1969, Wu et al 1973, 1979, Wallace et al 1983a, Watanabe & Endo 1991. Selenium deficiency also reduces testis size, and prolonged deficiency results in atrophy of the seminiferous epithelium (Sprinker et al 1971, Wallace et al 1983a, Behne et al 1996, MarinGuzman et al 2000.…”

Section: Introductionmentioning

confidence: 99%

Sequential development of flagellar defects in spermatids and epididymal spermatozoa of selenium-deficient rats

Olson¹,

Winfrey²,

Hill³

et al. 2004

Reproduction

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In this study cauda epididymal spermatozoa of rats maintained on a selenium-deficient diet for 5 and 7 months exhibited an array of flagellar defects. Spermatids and spermatozoa were analyzed by light and electron microscopy to define the appearance of flagellar abnormalities during spermiogenesis and post-testicular sperm development. Late spermatids of seleniumdeficient rats displayed normal structural organization of the flagellar plasma membrane, axoneme, outer dense fibers, fibrous sheath and annulus, but they exhibited a premature termination of the mitochondrial sheath. A comparison of late spermatids and caput epididymal spermatozoa revealed that a late step in flagellar differentiation was the structural remodeling of the annulus and its accompanying fusion with both the fibrous sheath and the mitochondrial sheath. In selenium-deficient animals, however, the annulus failed to fuse with the mitochondrial sheath, generating an apparent weak point in the flagellum. After epididymal passage, cauda epididymal spermatozoa of selenium-deficient animals also exhibited extensive flagellar disorganization resulting from the apparent sliding and extrusion of specific outer dense fiber-doublet microtubule complexes from the proximal and the distal ends of the mitochondrial sheath and the accompanying loss of the midpiece plasma membrane. Only fiber complex number 4 was extruded proximally, whereas fibers 4, 5, 6 and 7 were extruded from the mitochondrial sheath-deficient posterior midpiece. Axonemal fibers 8, 9, 1, 2 and 3 retained their normal geometric relationships. These data suggest that the known loss of male fertility in selenium deficiency results from the sequential development of sperm defects expressed during both spermiogenesis and maturation in the epididymis.

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Some Selenium Responses in the Rat not Related to Vitamin E

Cited by 167 publications

References 12 publications

Enhancement of epidermal growth factor (EGF) and insulin‐stimulated tyrosine phosphorylation of endogenous substrates by sodium selenate

Enhancement of epidermal growth factor (EGF) and insulin‐stimulated tyrosine phosphorylation of endogenous substrates by sodium selenate

Trace Elements and Electrolytes Homeostasis and Their Relation to Antioxidant Enzyme Activity in Brain Hyperexcitability of Epileptic Patients

Sequential development of flagellar defects in spermatids and epididymal spermatozoa of selenium-deficient rats

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