Elevated levels of aluminum have been reported in surface waters and in certain aquatic organisms including aquatic insects. Toxic effects have been demonstrated in fish and it has been suggested that aluminum affects avian reproduction. In this study Ringed Turtle-Doves were assigned to a control group fed a diet reduced in calcium and phosphorus and to a treated group fed the same diet supplemented with 0.1% aluminum. A 4-month feeding period with aluminum sulphate did not result in any effect on egg production, fertility, or hatchability. Egg permeability was decreased initially but subsequently recovered to a normal level. Dietary aluminum sulphate did not affect plasma calcium, phosphorus, or magnesium of adults nor did it affect the pattern of growth and the final weight of chicks feeding on the same diet. Bone aluminum levels of breeding females averaged twice those of the controls (P < 0.05). The pattern of accumulation between the two sexes was significantly different (P < 0.05). Growth of juvenile Ringed Turtle-Doves was not affected by dietary levels of aluminum sulphate up to 1500 ppm, although aluminum tended to accumulate in the bones of the sternum. No significant influence of aluminum on reproduction or growth, at levels similar to those likely to occur in the environment, could be found in the course of our laboratory experiment.

In 1982, 29 7-day-old American kestrel (Falco sparverius) chicks from captive stock were randomly assigned to one of three dietary regimens: (1) 10 birds were fed daily with cockerel mash (0 ppm of F-: control birds); (2) 10 birds were fed daily with cockerel mash containing 1,120 ppm of F-; (3) 9 birds were fed daily with cockerel mash containing 2,240 ppm of F-. Growth of the kestrels was not significantly affected by NaF in their diet. No significant differences were found among the 3 groups for length of duodenum, jejunum and ileum. Rectum was longer as more fluoride was added to the diet. Weights of adrenals, brain, gizzard, spleen, heart, kidneys, liver, pancreas, and pectoral muscle were not significantly affected by treatment, although kidneys, spleen and adrenals tended to become lighter. Percent bone ash was significantly (P less than 0.05) increased, while bone breaking strength was significantly (P less than 0.05) decreased by treatment.

Rationale: Intrauterine growth restriction (IUGR) increases the risk of bronchopulmonary dysplasia (BPD), one of the major complications of prematurity. Antenatal low-protein diet (LPD) exposure in rats induces IUGR and mimics BPD-related alveolarization disorders. Proliferator-activated receptor (PPARg) plays a key role in normal lung development and was found deregulated following LPD exposure. Objectives: Investigate the effects of nebulized curcumin, a natural PPARg agonist, to prevent IUGR-related abnormal lung development. Methods: We studied rat pups antenatally exposed to an LPD or control diet (CTL) and treated with nebulized curcumin (50 mg/kg) or vehicle from postnatal (P) days 1 to 5. The primary readouts were lung morphometric analyses at P21. Immunohistochemistry (P21) and microarrays (P6 and P11) were compared within animals exposed to LPD versus controls, with and without curcumin treatment. Results: Quantitative morphometric analyses revealed that LPD induced abnormal alveolarization as evidenced by a significant increase in Mean Linear Intercept (MLI) observed in P21 LPD-exposed animals. Early curcumin treatment prevented this effect and two-way ANOVA analysis demonstrated significant interaction between diet and curcumin both for MLI (F(1,39)=12.67,p=0.001) and Radial Alveolar Count at P21 (F(1,40)= 6.065, p=0.0182). Immunohistochemistry for FABP4, a major regulator of PPARg pathway showed a decreased FABP4+ alveolar cell density in LPD-exposed animals treated by curcumin. Transcriptomic analysis showed that early curcumin significantly prevented the activation of pro-fibrotic pathways observed at P11 in LPD-exposed animals. Conclusion: Nebulized curcumin appears to be a promising strategy to prevent alveolarization disorders in IUGR rat pups, targeting pathways involved in lung development.