Lack of dietary calcium effect on chlordecone increased white blood cell count, total iron, and iron-binding capacity in serum of rat.

Male Sprague-Dawley rats were treated with 0, 1, 10, 50, and 100 ppm of chlordecone (Cd) mixed in calcium-sufficient (Ca-S) or calcium-deficient (Ca-D) diet for 15 days. The control rats fed with Ca-D diet exhibited a significant increase in white blood cell (WBC) counts compared to the rats fed with Ca-S diet. Dietary calcium (Ca), however, did not elicit any significant effect on total iron content and iron-binding capacity (transferrin) of control rats, whereas Cd at higher concentrations significantly increased WBC counts, total iron, and iron-binding capacity in serum of both Ca-S and Ca-D rats. The data suggest that dietary Ca did not alter Cd-increased WBC count, total iron, and iron-binding capacity in serum of rat.

Influence of dietary calcium on chlordecone-induced biochemical changes in serum of rat.

Male, Sprague-Dawley rats were treated with different (1, 10, 50, and 100 ppm) concentrations of chlordecone (Cd) in calcium-sufficient (Ca-S) or calcium-deficient (Ca-D) diet for 15 days. No significant changes in serum total proteins were observed. However, serum nonprotein nitrogen compounds (urea, uric acid, and creatinine) and glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, creatine kinase, and alkaline phosphatase were significantly increased at 50 and 100 ppm of Cd. Chlordecone induced more increase in these serum components of rats fed with Ca-D as compared to Ca-S diet. Increased serum nonprotein nitrogen compounds and enzymes indicate Cd-altered glomerular and hepatic functions.

The effects of dietary calcium and chlordecone on cholinesterase, triglycerides, low density lipoproteins, and cholesterol in serum of rat.

Male, Sprague-Dawley rats were treated with 0, 1, 10, 50, 100 ppm chlordecone (Cd) mixed in calcium-sufficient (Ca-S) or calcium-deficient (Ca-D) diet for 15 days. A significant decrease in body weight gain was observed in 100 ppm of Cd-treated rats. Cholinesterase (ChE) activity was significantly decreased in serum of Ca-D rats. Chlordecone did not alter serum ChE activity in both Ca-S and Ca-D rats. However, Cd decreases serum triglycerides, low density lipoproteins (LDL) and cholesterol in both Ca-S and Ca-D rats. Rats fed with Ca-S or Ca-D diet exhibited differential sensitivity to Cd-toxicity. Decreased levels of serum triglycerides, LDL and cholesterol suggest that Cd might interfere in lipid metabolism.

Effects of chlordecone and malnutrition on immune response in rats.

Effect of Chlordecone (Cd) and malnutrition on total body and spleen weights, and plaque forming cells (PFC) were studied. Rats were fed on normal, calcium (Ca-D), protein (P-D) or Ca+P-deficient diets containing 0, 10 or 100 ppm of Cd for 2 or 4 weeks. High (95-100%) mortality was observed in malnourished rats treated with 100 ppm of Cd for 4 weeks. A slight decrease in body weight and an increase in spleen weight was observed in normal but not malnourished rats treated with 10 ppm of Cd for 4 weeks. PFC were significantly increased in both malnourished and Cd-treated rats. Similar increase in PFC was observed in rats fed on Ca-D but not P-D diet containing 10 or 100 ppm of Cd. Whereas, rats fed on Ca+P-D diet containing 100 ppm of Cd exhibited a significant decrease in PFC.

Changes in brain ATPases in rats fed on chlordane mixed with iron-sufficient and deficient diet.

The in vivo effects of chlordane on brain Na+-K+, oligomycin-sensitive (O.S) and oligomycin-insensitive (O.I) Mg2+ ATPases in rats were investigated. The rats were fed on 0, 25, 50 and 100 ppm chlordane mixed with iron-sufficient (I.S) and deficient (I.D) diets for 12 weeks. The enzyme activities were determined in the brain P2 fraction of rats at the end of 4, 8 and 12 weeks after treatment. Na+-K+ ATPase activity was reduced in a dose-dependent and time-dependent manner in rats fed on chlordane mixed with I.S and I.D diets. The reduction in the enzyme activity was more pronounced in the rats fed on chlordane mixed with I.D diet as compared to those fed on I.S diet. The brain O.S Mg2+ ATPase was also reduced in rats receiving chlordane. The reduction of O.S Mg2+ ATPase was higher than Na+-K+ ATPase. However, the O.I Mg2+ ATPase activity in rats fed on chlordane was not altered at any dose level. These results indicate that the rat brain ATPases may be particularly sensitive to chlordane.

Effect of cadmium on ATPase activities in rats fed on iron-deficient and sufficient diets.

Male Sprague-Dawley rats were fed on different levels of cadmium mixed with purified diets containing iron or no iron for 8 weeks. The body weight gain, tissue weights, hemoglobin, hematocrit, liver and brain ATPase were measured at 2, 4 and 8 weeks after feeding. The hemoglobin and hematocrit values were the same in all rats fed on cadmium. The rats fed on iron-deficient diets mixed with cadmium showed a significant decrease in body weight gain. However, the rats receiving only the 100 ppm of cadmium in iron-sufficient diet showed a significant decrease in body weight gain. There were no significant changes in the weights of thymus, spleen, kidney, heart, brain and testes. However, the liver weights were decreased in the highest treatment of cadmium but the liver weight/body ratios were uneffected. Na+-K+ activated ATPase activity in brains of rats fed on cadmium were significantly decreased at 2, 4 and 8 weeks of treatment. The decrease was more pronounced in rats fed on iron-deficient diets. Oligomycin-sensitive (Mitochondrial) Mg2+ ATPase activity was also significantly decreased in liver and brain tissues of rats fed on cadmium. Oligomycin-insensitive Mg2+ ATPase activity, however, was not altered in any tissues tested. It appears that cadmium may be interfering with energy (ATP) production and utilization processes in rat brain and liver tissues.

Cobalt induced changes in immune response and adenosine triphosphatase activities in rats.

The immuno-biochemical effects of cobaltous chloride in rats receiving iron-sufficient and deficient diets were investigated. Rats receiving 100 ppm or more cobalt showed a significant reduction in thymus and body weights along with a marked decrease in hemoglobin, hematocrit, sheep agglutinins and plaque forming cells. These effects were more pronounced in rats receiving cobalt mixed with iron-deficient diet than those fed on iron-sufficient diet. The Na+-K+ and mitochondrial (Oligomycin-sensitive) Mg2+ATPase activities in brain and liver of rats fed with iron-deficient diets were decreased significantly. However, the ATPase activities in these tissues from rats fed with cobalt mixed with iron-sufficient diets were not altered.

Inhibition of rat hepatic microsomal cytochrome P-450 system by cobaltous chloride and reversal of inhibition by iron in vivo.

The effects of preexposure of rats to cobaltous chloride (CO) mixed in iron-sufficient (I.S) and -deficient (I.D) diets on hepatic microsomal electron transfer system was investigated. Male Sprague-Dawley rats were fed for 4 weeks on I.D diets mixed with 0, 100 and 200 ppm CO. At the end of 4 weeks three rats from each group were transferred to I.S diets mixed with the same amount of CO. Liver microsomal NADPH - Cytochrome C reductase, NADPH - dehydrogenase, cytochrome P-450 and aniline binding were determined in both batches of rats. The rats receiving CO in the I.D diets showed a 35, 60, 75 and 40% decrease in NADPH - Cyt. C reductase, dehydrogenase, Cyt. P-450 and aniline binding respectively. The rats transferred from I.D diet to I.S diet showed a complete recovery of the inhibition of the microsomal electron transfer system. The rats receiving 200 ppm mixed with I.S diets did not show any changes in any biochemical parameter measured.