Effects of ammonium metavanadate on fertility and reproductive performance of adult male and female rats

Morgan, Ashraf M.; El-Tawil, Osama S.

doi:10.1016/s1043-6618(02)00241-4

Cited by 46 publications

(23 citation statements)

References 25 publications

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“…Intraperitoneal injections of rats with orthovanadate revealed nephrotoxicity [217]. The effect of vanadium on the reproductive and developmental functions in rats has also been well established [218]. Acute toxicity of vanadium compounds in animals involves dehydration, reduction of body weight, loss of appetite, renal tubular necrosis and pulmonary hemorrhage.…”

Section: Vanadiummentioning

confidence: 99%

Metals, Toxicity and Oxidative Stress

Valko

Morris²,

Cronin

2005

CMC

4,291

2,664

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Metal-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen and nitrogen species, is reviewed. Metal-mediated formation of free radicals causes various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulfhydryl homeostasis. Lipid peroxides, formed by the attack of radicals on polyunsaturated fatty acid residues of phospholipids, can further react with redox metals finally producing mutagenic and carcinogenic malondialdehyde, 4-hydroxynonenal and other exocyclic DNA adducts (etheno and/or propano adducts). Whilst iron (Fe), copper (Cu), chromium (Cr), vanadium (V) and cobalt (Co) undergo redox-cycling reactions, for a second group of metals, mercury (Hg), cadmium (Cd) and nickel (Ni), the primary route for their toxicity is depletion of glutathione and bonding to sulfhydryl groups of proteins. Arsenic (As) is thought to bind directly to critical thiols, however, other mechanisms, involving formation of hydrogen peroxide under physiological conditions, have been proposed. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. Common mechanisms involving the Fenton reaction, generation of the superoxide radical and the hydroxyl radical appear to be involved for iron, copper, chromium, vanadium and cobalt primarily associated with mitochondria, microsomes and peroxisomes. However, a recent discovery that the upper limit of "free pools" of copper is far less than a single atom per cell casts serious doubt on the in vivo role of copper in Fenton-like generation of free radicals. Nitric oxide (NO) seems to be involved in arsenite-induced DNA damage and pyrimidine excision inhibition. Various studies have confirmed that metals activate signalling pathways and the carcinogenic effect of metals has been related to activation of mainly redox-sensitive transcription factors, involving NF-kappaB, AP-1 and p53. Antioxidants (both enzymatic and non-enzymatic) provide protection against deleterious metal-mediated free radical attacks. Vitamin E and melatonin can prevent the majority of metal-mediated (iron, copper, cadmium) damage both in vitro systems and in metal-loaded animals. Toxicity studies involving chromium have shown that the protective effect of vitamin E against lipid peroxidation may be associated rather with the level of non-enzymatic antioxidants than the activity of enzymatic antioxidants. However, a very recent epidemiological study has shown that a daily intake of vitamin E of more than 400 IU increases the risk of death and should be avoided. While previous studies have proposed a deleterious pro-oxidant effect of vitamin C (ascorbate) in the presence of iron (or copper), recent results have shown that even in the presence of redox-active iron (or copper) and hydrogen peroxide, ascorbate acts as an antioxidant that prevents lipid peroxidation and does not promote protein oxidation in humans in vitro. Experimental results have also shown a link ...

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Section: Vanadiummentioning

confidence: 99%

Metals, Toxicity and Oxidative Stress

Valko

Morris²,

Cronin

2005

CMC

4,291

2,664

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“…The toxicity of vanadium is correlated to its degree of oxidation (vanadyl < vanadate ion) and chemical form (organic < inorganic ligand) [16,42]. This was demonstrated by experiments on animals, mainly in rats and mice [9,42,[60][61][62]. Its appears that both short-term (for a few days) and longterm (for a few months) administration of this element causes a variety of toxic effects such as hematological and biochemical changes (e.g.…”

Section: Toxicity Of Vanadiummentioning

confidence: 99%

Biological activity of vanadium compounds

Goc

2006

Open Life Sciences

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Vanadium compounds are characterised by a broad spectrum of action in vivo and in vitro. Their insulin-mimetic activity is manifested in their ability to normalize changes observed in both clinical and experimental diabetes (i.e. hyperglycaemia, hyperlipidaemia, lowered cell sensitivity to insulin) through the regulation of carbohydrate and lipid metabolism and the removal of secondary symptoms of this disease (as e.g. retinopathy, cardiomyopathy, nephropathy). Nevertheless, vanadium is considered to be a toxic element in both cationic and anionic form, although the latter type has more serious side effects. This is accounted for by the faster absorption of anionic forms, although the chemical structure, geometry, and the manner of synthesis of its derivatives also contributes to this elevated toxicity. Besides their antidiabetic properties, vanadium derivatives have also been observed to influence processes related to mitogenic cell responses (apoptosis, proliferation, neoplastic transformation). However, both anti-and pro-neoplastic properties of vanadium are reported.

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“…However, until recently little information is available about the male reproductive toxicity of vanadium compounds. The information obtained indicates that such effects are restricted to the testicle, sperm and hormonal regulation of spermatogenesis [16][17][18][19]. However, involvement of oxidative mechanisms in the toxic manifestations induced by vanadium compounds in male reproductive system is quite insufficient.…”

Section: Introductionmentioning

confidence: 99%