Thermoxidized palm oil induces reproductive toxicity in healthy and malnourished rats.

Repeatedly thermoxidized palm oil (TPO), simulating local culinary practice, was fed for eight weeks at 15% of a balanced basal diet to two sets of male and female weanling albino rats of Wistar strain. The first set of animals were normal and healthy while the second set were kwashiorkoric. Primary controls (PC) of all rats were fed a balanced basal diet of commercial rat pellets while secondary controls (SC) were fed the balanced basal diet supplemented with 15% untreated palm oil. The findings indicate that fertility, as expressed by the pregnancy rate of healthy test rats, was 78% when compared with 80% in PC (p < 0.05). Fetotoxicity was additionally observed in that neonatal birth weights and litter size in test rats (4.92 g and 6.70, respectively) were inferior (p < 0.05) to both SC and PC (4.96 g and 8.40; 5.38 g and 9.25, respectively). Protein energy malnutrition worsened the observed TPO-induced reproductive toxicities in that reproductive capacities of the rehabilitated animals were inferior to that of the healthy animals. Pregnancy rates in test animals were reduced by as much as 55% (p < 0.01) while fetotoxicities were also more pronounced (p < 0.05).

Abnormalities in adenosine triphosphatase of the erythrocyte membrane in iron deficiency anaemia.

During iron deficiency rat and human erythrocyte membrane enzyme activities (Total ATPase and Ouabainsensitive Na+.K+ ATPase) showed significant (P < 0.001) decrease. The influence of iron deficiency on erythrocyte Na+ and K+ was also studied in rats and humans. The former parameter showed a significant (P < 0.01) increase while the latter showed a downward trend. Plasma Fe and Total Iron Binding capacity (TIBC) in iron deficiency varied significantly (P < 0.05) from normal values. These results suggest a defect in erythrocyte membrane function and a possible potentiating effect of intracellular Na+, plasma Fe and TIBC on ATPase activity in iron deficiency. Values obtained for rats and humans showed differences in the activities of membrane ATPase in iron deficiency anaemia.

Transforming growth factor beta expression and transformation of rat lung epithelial cells by crystalline silica (quartz).

Crystalline silica (quartz) induces silicosis and associated peripheral lung carcinomas in rats. The role and pattern of expression of transforming growth factor (TGF)-beta1/beta2 mRNA transcripts were investigated in the fetal rat lung epithelial cell line FRLE, its neoplastic transformants and derived tumors in athymic nude mice. FRLE cells, treated with 100 microgram/cm2 of quartz in serum-free medium, gave rise to phenotypically altered, tumorigenic cells. Quartz-treated, transformed and tumorigenic cells, subcultured directly (QTT-C1) or after growth in soft agar (QTT-C2), formed tumors in athymic nude mice (QTT-T1). Cells subcultured from the tumors (QTT-T1C) were also tumorigenic in nude mice (QTT-T2). QTT-T1 and QTT-T2 tumors were poorly differentiated carcinomas with variable amounts of extracellular matrix-associated TGF-beta1 and desmoplasia. For comparison, a tumorigenic cell line derived from FRLE cells transformed with a mutated K-ras plasmid (RT-C1) and cells subcultured from a corresponding nude mouse tumor (RT-T1) and designated RT-T1C were used. Whereas TGF-beta1 and TGF-beta2 inhibited the growth of QTT-T1C and FRLE cells in a dose-dependent fashion, RT-T1C cells, containing an activated ras gene, were relatively unaffected. TGF-beta1 and TGF-beta2 mRNAs were expressed at higher levels in QTT-T1C cells than in FRLE and TR-T1C cells, and there was an increase in TGF-beta type II receptor (TGR-betaR) mRNA expression in QTT-T1C and RT-T1C cells compared to FRLE cells. Carcinomas in nude mice derived from QTT and RT cells and silicosis-associated lung carcinomas induced in rats by intra-tracheal quartz did not express either active or latent forms of TGF-beta1 protein on immunohistochemistry. The disparity between TGF-beta1 mRNA and TGF-beta1 protein expression in QTT tumors may be due to post-transcriptional regulation of TGF-beta1.

In vivo evaluation of iron bioavailability in some Nigerian peasant meals by haemoglobin regeneration technique.

The bioavailability of iron in three different rural Nigerian peasant meals was studied. The meals were: pounded yam (Discorea spp) with 'afia efere'--(plain soup); 'ekpang nkukwo'--grated cocoyam (Xanthosoma maffafa Schott) and cocoyam leaves with pepper and plantain porridge (Musa paradisiaca) with water leaf (Talinum triangulare). Analyses of the meals showed the protein content to range from 8.58 +/- 0.01 mg/100 g DM to 11.38 +/- 0.08/100g DM. Iron content ranged from 17.50 +/- 2.50 mg/100 DM to 23.94 +/- 3.56 mg/100g DM. The rehabilitation of mildly anaemic rats with test meals showed the percentage of the ingested iron utilised for haemoglobin synthesis as: 48.08 +/- 0.51 pc; 18.09 +/- 0.41 pc; 19.09 +/- 0.36 pc for the test diets respectively and 60.80 +/- 0.22 pc for the control group. A comparison of the utilization of iron between the test and the control groups showed that there was a significant difference (p < 0.01) between the test and the control groups. The low level of iron enhancers in the meals has been suggested as the possible cause of the marginal level of iron availability from the meals to the test animals.

Effects of fenfluramine on the metabolism of calcium and phosphorus in the rat: fenfluramine effects on Ca and P metabolism.

Daily administration of 2, 5, 10, 15 and 20mg of fenfluramine/kg body weight to adult rats for four weeks resulted in dose dependent decrease in calcium and phosphorus absorption with an inverse correlation of r = -0.94 for calcium and r = -0.93 for phosphorus. Significant (P less than 0.05) increase in the total faecal lipids and moderate decline in plasma calcium levels were also observed in the rats. Adult rats made obese by dietary methods when treated with 10mg and 15 mg of fenfluramine/kg body weight/day for 10 weeks showed a significant reduction (p less than 0.001) in the intestinal absorption of both calcium and phosphorus. The reduction at 15mg/kg drug dose was 10.7 pc for calcium and 9.5 pc for phosphorus. Analyses of the long bones as well as carcasses of the obese rats showed significant decrease (p less than 0.001) in the content of these minerals. Plasma calcium and phosphorus levels were also significantly (p less than 0.001) reduced in the obese-treated rats. However, fenfluramine treatment significantly reduced the plasma calcium but not the phosphorus levels in the non-obese rats. These studies have demonstrated that chronic administration of fenfluramine (greater than or equal to 10mg/kg body weight) to rats, obese or non-obese, impairs calcium and phosphorus metabolism in the body.

Electrolytes (Na+ and K+) translocation in erythrocytes during iron deficiency in rats and humans.

During iron deficiency a significant (p less than 0.01) increase in erythrocyte Na+ in vivo was observed in both rats and humans. Erythrocyte K+ was down, but the effect was only significant (p less than 0.05) in rats, under this condition. However, erythrocyte Na+/K+ ratio was significantly (p less than 0.001) higher in iron deficiency when compared to normal values in both rats and humans. Although there was no significant (p greater than 0.05) correlation between Haemoglobin (Hb), Packed cell volume (PCV), Plasma Fe, and Total Iron Binding capacity (TIBC), and erythrocyte Na+ or K+ levels during iron deficiency, analysis of variance showed that Hb, PCV, Plasma Fe and TIBC in concert significantly (p less than 0.05) affected erythrocyte Na+ in iron-deficient rats and humans, whereas K+ was significantly (p less than 0.05) affected only in rats. These studies suggest a defect in erythrocyte membrane function during iron deficiency and imply a concerted potentiating effect of Hb, PCV, Plasma Fe and TIBC on erythrocyte membrane malfunction during iron deficiency. Species difference is also demonstrated in erythrocyte (Na+ and K+) translocation in iron deficiency.