Characterization of the postmortem biochemical changes and the electrogenic transepithelial ion currents in rat colon-as possible markers for determination of time of death

Many biochemical studies of the experimental postmortem interval estimation were carried out on tissues incubated in vitro after extirpation. Because the extirpation affects cell viability, we investigated the changes in cathepsin D [cat D], lactate dehydrogenase [LDH], acid phosphatase [AcP] and alkaline phosphatase [ALP] activities and nucleic acids [DNA and RNA] content in the colon tissues of male Wistar rats occurring postmortem in situ in relation to time passed since death. Also, the postmortem transepithelial ion currents elecited by forskolin stimulation of rat colon were examined. The results showed significant and transient increase in cat D, AcP and LDH activities as early as 1 hr after death compared to control group [0 hr]. They reached the peak at 3, 6 and 9 hrs postmortem, respectively, then began to decrease at 6, 9 and 24 hrs, respectively till reached below control values at 72 hrs postmortem. On the other hand, ALP activity and nucleic acids content showed significant and permanent reduction beginning after 1 and 9 hrs postmortem, respectively. The maximum reduction was noted at the end of experiment [72 hrs postmortem]. The obtained results revealed also that the addition of forskolin to the serosal side of stripped rat colon at 0, 3 and 6 hrs postmortem induced a dose-related elevation in the short circuit current [SCC]. Following the next times 9 and 24 hrs, there was an increase in Kd and a decrease in Jmax with failure of response after 24 hrs. In conclusion, our results revealed that cat D, AcP, ALP and LDH activities and electrogenic ion current response of the colon to forskolin are usuefull markers for estimating time after death within the postmortem interval of 1-24 hrs. However, the changes in the nucleic acids content were correlated with the time elapsed since death during postmortem period of 1-72 hrs and can be used to estimate longer times passing after death

Immunotoxic effects of lambda-cyhalothrin in rabbits

The effect of Lambda-cyhalothrin on the immune response was studied in rabbits exposed to the insecticide via food at concentrations of 1373.23, 686.76 or 343.38 ppm [equivalent to 1/10[th], 1/20[th] and 1/40[th] oral LD50, respectively] for 8 weeks. The humoral immune response was measured by determination of the antibody titre against sheep red blood cells [SRBC], a T - cell dependent antigen. Moreover, the cell-mediated immune response was evaluated by the delayed - type hypersensitivity reaction to tuberculin. The chemical treatment resulted in a dose - dependent suppression of both humoral and cellmediated immune responses as evidenced by decreased serum hemolysin titres and inhibition of the delayed-type hypersensitivity reaction to tubercluin, respectively. In addition, leucopenia, lymphopenia, depletion of lymphoid cells in the white pulps of spleen, mesentric lymph nodes and Peyer's patches and severe atrophy of thymus cortex were recorded. The serum total protein, albumin, globulin [specially gamma globulin], albumin/globulin [A/G] ratio and the organ to body weight ratios for spleen and thymus were significantly decreased with increasing the insecticide dosage. Moreover, different pathological alterations in liver, and brain were also observed. In conclusion, Lambdacyhalothrin exposure suppressed both humoral and cell-meditated immune responses in rabbits at the tested concentrations in a dose - dependent manner

Developmental toxicity evaluation of oral aluminum in rats

The present study was designed to elucidate the adverse effects of the orally administered aluminum [Al] on the growing fetus and consequently on the animal wealth in our country. This aim has been achieved by studying the teratogenic, perinatal and postnatal effects of aluminum chloride when administered orally at 345 mg/kg body weight to female rats during organogenesis, fetal and/ or lactation periods. The results showed that Al chloride exposure on days 6-15 of gestation produced a significantly higher percentage of postimplantation death, resorptions, morphological, visceral and skeletal anomalies in the obtained fetuses compared to the control group. In addition, the live fetuses' percentage, mean fetal body weight and placental weights were significantly decreased. The obtained data revealed also that Al chloride exposure on 6[th] day of gestation till weaning induced significant increase in the percentage of dams showed delayed birth date and signs of dystocia. In addition, it induced a significant increase in the percentage of postimplantation loss, dead fetuses; fetuses showing neurobehavioral and respiratory symptoms and those born with morphological abnormalities. Moreover, it decreased the live/ birth, survival and viability indices and weight gain of these fetuses compared with control. The Al- induced effects on the obtained fetuses from Al chloride treated dams through lactation period included significant increase in the percentage of postnatal deaths, fetal stunted growth with a significantly increased percentage of nervous and respiratory symptoms prior to death. Consequently, the survival and viability indices were reduced. Moreover, the weight gain during lactation was significantly reduced. Brain examination of the obtained fetuses from all exposed dams throughout this study showed different histopathological changes. It can be concluded that Al chloride exposure of female rats during gestation and/ or lactation periods caused teratogenic, perinatal and postnatal adverse effects on their progeny

Teratogenic effect of the coumarinic anticoagulant rodenticide, racumin in white rats

The present study gives an overview of the in utero exposure of the developing rat fetus to Racumin rodenticide. In the current investigation, pregnant rats were exposed orally to either 1.65 or 0.83 mg/kg b.wt [1/10 and 1/20 LD50, respectively] of coumatetralyl daily on days 6 through 15 of gestation [organogenesis period]. Maternal and fetal parameters were evaluated on day 20 of gestation. Fetuses were weighed and examined for external, visceral and skeletal malformations. Exposure to this rodenticide at the two tested doses significantly increased the number of resorption and implantation sites [post implantation loss], dead fetuses' number per dam and placental weights. The number of live fetuses per dam and the fetal body weight were significantly reduced in the treated group at 1.65 mg/kg b.wt.when compared to the other treated and control groups. Gross examination of the fetuses from Racumin treated dams' at both doses revealed significant incidences of dwarfism, subcutaneous hemorrhages, generalized subcutaneous edema and micrognathia. Racumin significantly increased the total fetuses with visceral and skeletal anomalies in a dose - dependent manner compared to the control. The major anomalies recorded were intrathoracic hemorrhage, hydrocephaly, heart and lung hypoplasia, anophthalmia, incomplete ossification of skull, sternebrae and coccygeal vertebrae. It could be concluded that Racumin has a dose - dependent teratogenic potential in rats

Potential protective effect of grape seed extract against acrylonitrile-induced mutagenicity in rats

Acrylonitrile [ACN], an environmental toxic pollutant, has been detected in drinking water, food products and occupational environment. ACN is reported as a potent in vivo and in vitro mutagen and carcinogen in human and experimental animals. Grape seed proanthocyanidine extract [GSE] is a highly bioavailable biologically active polyphenolic bioflavonoid. It is a potent antioxidant posses a broad spectrum of pharmacological and therapeutic activities against free radicals, DNA damage and oxidative stress. The objective of the present study was to investigate the possible in vivo protective effects of GSE against ACN-induced micronucleus and chromosomal aberrations in male rats. Animals were exposed to a single s/c dose of ACN [115 mg/kg body weight]. Another two groups of animals were pretreated with GSE in a dose of 100 and 200 mg/kg body weight orally for seven consecutive days prior to ACN administration [single s/c dose of 115 mg/kg body weight]. The animals were subjected to cytogenetic analysis in bone marrow by micronucleus induction and chromosomal aberrations assays. The present results indicate that ACN significantly induced micronuclei and chromosomal aberrations. Pretreatment with GSE significantly improved these mutagenic effects in a dose related manner

Protective effects of ascorbic acid and selenium against ammonium metavanadate-induced male reproductive toxicity in rats

The possible protective effects of ascorbic acid and/or selenium against the male reproductive toxicity of a pentavalent inorganic vanadium compound were investigated in male rats. Seven groups of adult rats, 20 rats each, were used in this experiment. The first group received untreated drinking water and served as control. The 2[nd] group received drinking water treated with ammonium metavanadate. The 3[rd] and 4[th] groups were given ascorbic acid and sodium selenate, respectively. However, the 5[th] 6[th] and 7[th] groups received the same ammonium metavanadate treated drinking water and given ascorbic acid; sodium selenate; ascorbic acid + sodium selenate, respectively. Ammonium metavanadate was administered via drinking water at a concentration of 200 ppm. However, ascorbic acid and sodium selentate were given orally at daily doses of 250 and 0.5 mg/kg b.wt, respectively. Both treated and control animals were sacrificed at the 35[th] and 70[th] days for studying the effects of vanadium and vanadium protectors on sex organs, sperm parameters and testicular biochemistry. Our results revealed that ammonium metavanadate exposure resulted in decreased weight of sex organs; pathological changes in testes, epididymis and prostrate and biochemical alterations in the testicular glycogen content, cholesterol level and acid and alkaline phosphatase activities. Moreover, hypospermia, increased abnormal and deal sperms and decreased sperm motility were also recorded. On the other hand ascorbic acid and sodium selenate supplementation produced variable degrees of protection. The protective effects of ascorbic acid were observed in the weight changes of sex organs; pathological changes in the testes, epididymis and prostate gland; sperm parameters and testicular biochemistry. Selenium induced a lesser degree of protection in the studied parameters than ascorbic acid and there was mild histopathological changes in the testes, epididymis and prostate. However the use of a combination of both ascorbic acid and selenium offered the best degree of protection. In conclusion, administration of ascorbic acid and sodium selenate had significant protective effects on the male reproductive system of rats especially the testes against vanadium - induced oxidative damage and the use of a combination of both ascorbic acid and selenium provides the better protection than when each one given alone