Biomedical subjects

O Ademuyiwa

Publications and source records attributed to O Ademuyiwa.

6 recordsLinked to original sources

PubMed2002

Zinc in CCl4 toxicity.

OBJECTIVE: To investigate the protective effect of zinc in CCl4-induced hepatotoxicity. METHODS: Rats were treated with zinc acetate for four days. The zinc doses were 5 mg Zn/kg and 10 mg Zn/kg body weight respectively. Two groups of the zinc acetate-treated rats were later challenged with a single dose of CCl4 (1.5 mL/kg body weight). RESULTS: Compared to control animals, the plasma of rats treated with CCl4 showed hyperbilirubinaemia, hypoglycaemia, hypercreatinaemia and hypoproteinaemia. When the animals were however supplemented with zinc in form of zinc acetate before being dosed with CCl4, the 5 mg Zn/kg body weight of zinc acetate reversed the hypoproteinaemia induced by CCl4, whereas the 10 mg Zn/kg body weight of zinc acetate reversed the hypoglycaemia, hyperbilirubinaemia and hypercreatinaemia induced by CCl4. CONCLUSION: The 10 mg Zn/kg body weight of zinc acetate is more consistent in protecting against CCl4 hepatotoxicity. The possible mechanisms of protection are highlighted.

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PubMed2000

Time course of arsenite-induced copper accumulation in rat kidney.

Oral administration of inorganic arsenic has been shown to lead to an accumulation of copper in the kidneys of rats and guinea pigs. However, nothing is known about the characteristics and mechanisms of this organ-specific renal copper accumulation. Many heavy metals accumulate in the kidney, either after environmental or occupational exposure. An additional accumulation of any other trace metals, even essential ones, may therefore be critical for that organ. This prompted us to follow the course of the renal copper accumulation. Rats were given daily subcutaneous doses of sodium arsenite for 12 d. Each second day, three rats were killed by exsanguination and the liver, kidneys, and blood removed and analysed for As, Cu, and other trace elements by atomic emission spectrometry. Results indicate that arsenic and copper accumulate in the kidney cortex synchroneously over time. Arsenic also accumulated in the liver and red blood cells (RBC). Copper levels in the RBC and liver as well as copper excretion into the urine were unaffected. After terminating arsenite administration, there was a slow decline in tissue levels of both arsenic and copper, a phenomenon which was parallel for both metals. Because the copper level in the liver was not affected, it is concluded from this study that renal processes and not hepatic or biliary mechanisms might be responsible for the renal copper accumulation. Furthermore, the strong linear correlation (r = 0.85) between arsenic and copper levels in the kidney during and after arsenite administration suggests a functional relationship between arsenic and copper with respect to their retention in the kidney.

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PubMed1999

Species differences in arsenic-mediated renal copper accumulation: a comparison between rats, mice and guinea pigs.

1. Administration of arsenite leads to an accumulation of copper in the rat kidney. Owing to the high retention of arsenic in the erythrocytes, however, the rat is considered to possess special toxicokinetics of arsenic and is therefore considered less comparable with other species in this respect. 2. Therefore, we compared the effect of dietary arsenite in mice and guinea pigs with that in rats. Each species was divided into four groups of animals according to the diets fed which contained increasing concentrations of sodium arsenite (NaAsO2; 0, 10, 30 and 60 mg As/kg of diet). Animals were killed after 1, 2 and 3 weeks. Tissues were sampled and analyzed for arsenic and other trace metals (Cu, Fe, Zn and Mn). 3. Compared to controls with copper levels of about 10 microg Cu/g wet wt. in the renal cortex, dietary administration of arsenite up to 60 mg As/kg of diet for 3 weeks to rats increased cortical levels to 65 microg Cu/g wet wt. An increase of renal copper levels similar to that in rats, was only observed in guinea pigs but not in mice. Renal copper accumulation in guinea pigs was time- and concentration-dependent as in rats. Feeding a diet with 60 mg As/kg for 3 weeks increased cortical copper levels from about 6 - 40 microg Cu/g wet wt. Renal copper levels in mice as well as other trace metal levels in guinea pigs and mice were not essentially altered by dietary arsenite. 4. The study shows that the renal copper-arsenic interaction is not restricted to the rat. Since in rats and guinea pigs, but not in mice, arsenic accumulated in the kidney rather similarly, a common mechanism is suggestive. As it was previously shown in rats that only inorganic arsenic is involved in this interaction, a rapid conversion of the inorganic form into methylated metabolites as in mice may diminish the extent of the renal copper accumulation whereas the lack of, or a less efficient, methylation as in guinea pigs or rats increases it.

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PubMed1996

Arsenic-copper interaction in the kidney of the rat: influence of arsenic metabolites.

The present study was an attempt to investigate whether the renal accumulation of Cu observed in the kidneys of rats and guinea-pigs exposed to arsenite (As-III) was an effect of arsenite alone or also shared by its metabolites--arsenate (As-V), dimethylarsinic acid and monomethylarsonic acid. The four arsenic compounds were administered subcutaneously and separately to rats for 12 days in increasing doses. Kidney, liver and blood were taken and analysed for As, Cu and other trace elements by atomic emission spectrometry. Results indicate that administration of As-V leads to renal Cu accumulation similar to that observed on administration of As-III and that the accumulation in both cases is dependent on the dose of arsenic, although higher doses of As-V were required to achieve renal Cu levels comparable to that of As-III. A constant molar As:Cu ratio independent of arsenic dose was obtained in the kidney. Dimethylarsinic acid did not affect renal Cu levels at all. Administration of monomethylarsonic acid led to a slight increase in renal Cu levels which did not increase further in spite of increased doses of monomethylarsonic acid. It is concluded from these studies that neither the metabolic transformation of inorganic arsenic to its methylated products nor its metabolites (dimethylarsinic acid and monomethylarsonic acid) caused the observed renal Cu accumulation, rather, the inorganic form of As, either in the trivalent or pentavalent form is responsible.

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PubMed1994

Vitamin C in CC14 hepatotoxicity--a preliminary report.

1. The hepatotoxic effect of CC14 was studied in the rat by using 3 well established liver function tests (plasma glucose, bilirubin and proteins) as indices of hepatic integrity. 2. The protective effect of vitamin C against this hepatotoxicity was also investigated. 3. CC14 (8 ml kg-1 body weight) caused a decrease in the levels of plasma conjugated bilirubin, glucose and protein. 4. Vitamin C (2 g kg-1 body weight) prevented liver damage induced by CC14. The possible mechanisms of protection are highlighted.

Animals↗

PubMed1990

Vitamin E and selenium in gentamicin nephrotoxicity.

1. The sequence of renal cellular membrane damage induced by gentamicin was studied in the rat by using the release of alkaline phosphatase, acid phosphatase, muramidase and protein from renal cells as indices of renal damage. 2. The protective effect of a combination of vitamin E and selenium against renal damage was also investigated. 3. Gentamicin (60 mg kg-1 body weight) was nephrotoxic within 12 h of the first dose. 4. The plasma membrane of the renal tubules is damaged before the lysosomal membrane is affected. 5. A combination of vitamin E (1 mg g-1 body weight) and selenium (4 x 10(-3) mg g-1 body weight) attenuates the renal damage induced by gentamicin. Results suggest synergism between vitamin E and selenium in attenuating the renal damage. The possible mechanism of attenuation is discussed. 6. Vitamin E and selenium may have anti-diuretic potential.

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