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A Marzuki

Publications and source records attributed to A Marzuki.

12 recordsLinked to original sources
PubMed1997

The oral and intratracheal toxicities of ROUNDUP and its components to rats.

The toxicities of ROUNDUP and its component chemicals, glyphosate (N-phosphonomethylglycine) and polyoxyethyleneamine (POEA), were determined at 0, 1, 3, 6 and 24 h following administration to rats. The intratracheal administration of glyphosate (0.2 g/kg), POEA (0.1 g/kg), a mixture of glyphosate (0.2 g/kg) + POEA (0.1 g/kg), or ROUNDUP (containing 0.2 g/kg glyphosate and 0.1 g/kg POEA) elicited immediate respiratory effects which were more severe and which lasted longer in the groups receiving the POEA-containing preparations than in the glyphosate alone group. By 1 h, all test preparations had caused deaths, but more occurred from the POEA-containing preparations than from glyphosate. The po administration of POEA (1 g/kg), the mixture of glyphosate (2 g/kg) +POEA (1 g/kg), or ROUNDUP (containing 2 g/kg glyphosate and 1 g/kg POEA) produced diarrhea and blood-stained weeping from noses. Death was only seen from POEA at 24 h. Glyphosate (2 g/kg po) produced transient diarrhea without nose bleeds; POEA caused diarrhea at 1 h; and the mixture of POEA + glyphosate produced diarrhea later that increased in severity with time. Bloody nose secretions were seen only with the preparations that contained POEA. No deaths, respiratory effects or bloody nose secretions occurred in controls given saline. Both POEA and glyphosate caused lung hemorrhages and lung epithelial cell damage with po or intratracheal exposures. These results indicate POEA and preparations that contained POEA were more toxic than glyphosate.

Administration, Oral↗
PubMed1996

Nitrofurantoin-induced hepatic and pulmonary biochemical changes in mice fed different vitamin E doses.

The hepatic and pulmonary effects of nitrofurantoin (40 mg/kg, intraperitoneally) were determined at 4 and 24 hr following its administration in mice fed for 10 weeks with a vitamin E sufficient, deficient or enriched diet. Liver glutathione (GSH) was reduced by nitrofurantoin at 4 hr but was unchanged 20 hr later. Nitrofurantoin did not affect liver glutathione peroxidase, glutathione reductase or superoxide dismutase activities. Liver catalase activities were decreased by nitrofurantoin at 4 hr. Lung GSH levels were increased whilst glutathione peroxidase activity was decreased at 4 and 24 hr. Lung glutathione reductase activity was reduced in certain groups. Nitrofurantoin did not affect lung superoxide dismutase, but catalase was decreased at 24 hr. Liver malondialdehyde levels were increased by nitrofurantoin in the vitamin E deficient group whilst lung malondialdehyde levels remained unchanged. Both liver and lung malondialdehyde levels were unaffected by vitamin E supplementation when compared to the vitamin E-sufficient group. These results suggest that nitrofurantoin (40 mg/kg) was deleterious to the liver and lung. Nitrofurantoin-induced lipid peroxidation was seen in vitamin E deficiency but an increase in dietary vitamin E content did not provide additional protection compared to the recommended daily allowance. The antioxidant activities of alpha-tocopherol and gamma-enriched tocotrienol were similar.

Animals↗
PubMed1993

Glutathione S-transferase and gamma-glutamyl transpeptidase activities in cultured rat hepatocytes treated with tocotrienol and tocopherol.

1. The effect of tocotrienol and tocopherol on glutathione S-transferase (GST) and gamma-glutamyl transpeptidase (GGT) activities in cultured rat hepatocytes were investigated. 2. Tocotrienol and tocopherol significantly decreased GGT activities at 5 days in culture but tocotrienol also significantly decreased GGT activities at 1-2 days. 3. Tocotrienol and tocopherol treatment significantly decreased GST activities at 3 days compared to the control but tocotrienol also decreased GST activities at 1-3 days. 4. Tocotrienol showed a more pronounced effect at a dosage of greater than 50 microM tocotrienol at 1-3 days in culture compared to the control.

Animals↗
PubMed1991

Influence of dietary fat on plasma lipid profiles of Malaysian adolescents.

We studied the effects of saturated (palm olein) and polyunsaturated (soybean oil) cooking oils on the lipid profiles of Malaysian male adolescents eating normal Malaysian diets for 5 wk. Diets cooked with palm olein did not significantly alter plasma total-cholesterol, LDL cholesterol, and HDL cholesterol concentrations or the ratio of total cholesterol to HDL cholesterol compared with diets cooked with soybean oil. However, the diet cooked with palm olein significantly increased apolipoprotein A-I (11%) and apolipoprotein B (9%) concentrations. Unexpectedly, soybean-oil-cooked diets caused a significant increase (47%) in plasma triglycerides compared with palm-olein-cooked diets. We conclude that palm olein, when used as cooking oil, has no detrimental effects on plasma lipid profiles in Malaysian adolescents.

Adolescent↗
PubMed1991

Effect of tocotrienols on hepatocarcinogenesis induced by 2-acetylaminofluorene in rats.

The effects of tocotrienols on hepatocarcinogenesis in rats fed with 2-acetylaminofluorene (AAF) were followed morphologically and histologically for a period of 20 wk. No differences between treated and control rats in the morphology and histology of their livers was observed. Cell damage was extensive in the livers of AAF-treated rats but less extensive in the AAF-tocotrienols-treated rats when compared with normal and tocotrienols-treated rats. 2-Acetylaminofluorene significantly increases the activities of both plasma and liver microsomal gamma-glutamyltranspeptidase (GGT) and liver microsomal UDP-glucuronyltransferase (UDP-GT). Tocotrienols administered together with AAF significantly decrease the activities of plasma GGT after 12 and 20 wk (P less than 0.01, P less than 0.002, respectively) and liver microsomal UDP-GT after 20 wk (P less than 0.02) when compared with the controls and with rats treated only with tocotrienols. Liver microsomal GGT also showed a similar pattern to liver microsomal UDP-GT but the decrease was not significant. These results suggest that tocotrienols administered to AAF-treated rats reduce the severity of hepatocarcinogenesis.

2-Acetylaminofluorene↗
PubMed1984

Effects of saturated and unsaturated dietary fat on aflatoxin B1 metabolism.

Male Fisher 344 rats were fed diets containing either 20% corn oil, 20% coconut oil or 18% coconut oil plus 2% corn oil for 3 wk. A single dose of [3H]aflatoxin B1 [(3H]AFB1) was administered ip and the biliary excretion of aflatoxin metabolites and the binding of 3H to nucleic acids were studied. In other experiments the in vitro metabolism of AFB1 by liver postmitochondrial supernatants prepared from rats fed the different sources of dietary fat was determined. The major nonextractable aqueous metabolite of AFB1 was the aflatoxin B1-glutathione conjugate (AFB1-GSH). Variation in the source of dietary fat did not affect production of the conjugate, nor was in vivo binding of AFB1 to nucleic acids affected. Aflatoxin P1 ( AFP1 )--mostly conjugated--and aflatoxin M1 (AFM1) were also identified in the bile, and the quantities of these metabolites produced were unaffected by the dietary treatments. The metabolites recovered in the in vitro study included aflatoxins Q1, P1 and M1. The corn oil diet produced a higher microsomal cytochrome P-450 level than the coconut oil diet. Associated with the higher level of cytochrome P-450 was increased in vitro conversion of AFB1 to AFQ1 and AFM1, but not to AFP1 . The in vitro production of aqueous metabolites and the covalent binding of metabolites to protein was unaffected by the dietary treatments. The results of the in vivo and in vitro studies suggest that the formation of the putative carcinogenic metabolite, AFB1-epoxide, which undergoes detoxification through glutathione conjugation, is not affected by the type of dietary fat. These observations further suggest that dietary fat, in particular unsaturated fat, affects AFB1 carcinogenesis through a mechanism other than by alteration of the metabolic activation of AFB1.

Aflatoxin B1↗
PubMed1984

Effects of dietary saturated or polyunsaturated fat on hepatic glutathione S-transferase activity.

Microsomal mixed function oxidases (MFO) responsible for phase I xenobiotic metabolism are partially dependent on dietary polyunsaturated fat. The reduced activity of the MFO when fat-free or saturated fat diets are fed has been associated with alterations of microsomal phospholipid fatty acid content. Glutathione S-transferases (GSH-transferases) catalyze phase II conjugation reactions, and are important detoxification pathways for highly reactive phase I-produced intermediates. We hypothesized that activity of membrane-bound, but not soluble, GSH-transferases would be affected by type of dietary fat. Rats were fed diets that contained either 20% coconut oil, 20% corn oil, or a mixture of 18% coconut oil plus 2% corn oil as the sole source of dietary fatty acids. At the end of the 3-week feeding period the activity of both microsomal and soluble fraction GSH-transferases of rat liver was determined. The original hypothesis that dietary fat type would alter membrane-bound transferase activity was not supported by the results since GSH-transferase activity in the microsomal fraction was not affected. However, feeding 20% coconut oil produced a 25 to 40% decrease in soluble transferase activity compared to corn oil feeding. The Michaelis constant (Km) for soluble GSH-transferase was threefold higher when the diet was devoid of polyunsaturated fat. Ultrafiltration of the soluble fraction to remove compounds with molecular weights below 50,000 did not eliminate the differences in transferase activity due to dietary fat. Separation of the soluble transferases by fast protein liquid chromatography indicated that quantities of the various transferases were affected equally by type of dietary fat. The results indicate that type of dietary fat may be important in determining the ability to detoxify carcinogens or other toxins that are conjugated with glutathione.

Animals↗
PubMed1971

Septic abortions.

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Abortion, Illegal↗