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There is a dearth of information on the mutual interaction between metal intoxication and adipocere formation. Herein, 40 adult female albino rats were distributed into two equal groups, one used as control while the other orally administered single dose of cadmium chloride (CdCl2) 225 mg/kg·bw (LDmin). Control group was killed by cervical dislocation. Half of dead rats of both groups were subjected for determination of iodine value and estimation of cadmium (Cd) residues while the other half of both groups were submerged in opened glass container previously filled with 4 L dechlorinated tap water kept in closed room with an open air access (one cadaver/container). Gross morphological changes of submerged cadavers were recorded weekly along the experiment. At the end of the experiment, after 3 months, samples were collected again for iodine value determination and estimation of Cd residues. The obtained results revealed the depressant effect of Cd toxicity on development of adipocere. Cd residues were found in different tissues of cadavers at time of death with the highest amount in the intestines followed by the liver and kidneys, then lungs, adipose tissue, muscles, and finally the bones. After 3 months of water submersion, tissues exhibited significant decrease in the amount of Cd residues but to a limit that was still detected. This study concluded the possibility of detection of Cd residues even after adipocere formation. Additionally, it shed light on the possibility of the interference of environmental pollution with the natural rate of decomposition especially adipocere formation. [ABSTRACT FROM AUTHOR]

Our present trial was carried out to investigate the hematological and immune related impacts of fenpropathrin (FNP) pyrethroid in male rats and to assess the ameliorating effect of camel milk (CM). Sixty male rats were randomly separated into six equal groups (n=10). 1st control (C), 2nd corn oil (CO), 3rd camel milk (CM) groups were orally gavaged physiological saline, CO, and CM respectively at doses of 2ml/rat day after day for 60 days. 4th (FNP treated group); orally received FNP 7.06 mg/kg B.W, 5th (CM+FNP pro/co treated group); received CM two weeks prior to and along with FNP, and 6th (FNP+CM co treated group); received FNP followed by CM with the same previous doses, route, and duration. FNP intoxication significantly decreased RBC counts, HCT, MCHC, Hb content, phagocytosis %, phagocytic index, serum lysozyme activity, and IgM levels. Also, FNP significantly increased leukogram, platelet count, TNFα and IL6 serum levels. CM significantly attenuates the altered indices more significantly in the (CM+FNP pro/co treated) group than the (FNP+CM co treated) group. Spleen tissues of FNP treated group revealed marked atrophy and lymphoid elements depletion with apoptosis. Furthermore; marked atrophy of thymic cortex, delineation of cortex and medulla with multifocal lymphocytic depletion. It is concluded that CM significantly attenuates both hematological and immunological toxic impacts induced by FNP oral intoxication in rats. Additionally CM pre and concurrent oral administration could lessen FNP induced alterations than CM concurrent administration only. [ABSTRACT FROM AUTHOR]