Dietary influence of kefir on microbial activities in the mouse bowel.

AIMS: In this work the microflora present in kefir, a fermented milk product, was studied together with the effect of kefir administration on different groups of indigenous bacteria of mouse bowel. METHODS AND RESULTS: Kefir microflora was composed of lactic acid bacteria, acetic acid bacteria and yeasts. Yeast population was composed of Saccharomyces cerevisiae, S. unisporus, Candida kefir, Kluyveromyces marxianus and K. lactis. The streptococci levels in kefir treated mice increased by 10-fold and the levels of sulfite-reducing clostridia decreased by 100-fold. The number of lactic acid bacteria increased significantly. CONCLUSIONS: The administration of kefir significantly increased the lactic acid bacteria counts in the mucosa of the bowel. Ingestion of kefir specifically lowered microbial populations of Enterobacteriaceae and clostridia. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first long-term study about the effects of the kefir administration on the intestinal microflora of mice.

Neurochemical changes in newborn rat's brain after gestational cadmium and lead exposure.

Gestational administration of cadmium (10 mg/l) and lead (300 mg/l) produced a strong decrease in proteins at birth (-17%) and on day 5 (-31%) as well as in brain lipid amount on both days (-11 and -23%, respectively). At day 5 postnatal the exposure also produced a marked decrease in DNA and RNA concentrations with respect to the control group. On the other hand, we found a significant increase of indoleamine content in all brain areas studied in the cadmium-lead group and so the dopamine and its metabolite in mesencephalon, whereas dopamine levels in metencephalon decreased significantly. This data suggests that gestational and early lactational exposure to low dose of cadmium and lead could produce alterations in monoaminergic metabolism that can place the exposed animal to a significant risk in adulthood.

Study of alterations produced by cadmium and cadmium/lead administration during gestational and early lactation periods in the reproductive organs of the rat.

Administration of cadmium (10 mg/liter) and cadmium+lead (300 mg/liter) via drinking water to Wistar rats during gestation and early lactation until delivery and (5 days after parturition) damaged pup reproductive systems. The effects are additive in the decreased gonad weight and additive or even synergistic in the reduced DNA gonadal content. The effects on protein reduction are similar for both cations. In the testes, the effects of cadmium are more important in the reduction of seminiferous tubule diameter, whereas the effects of lead are more overt in the reduction of the number of prospermatogonia.

Gestational administration of cadmium alters the neurotransmitter levels in newborn rat brains.

The effects of gestational and early lactational intoxication by cadmium (Cd) were studied in the brain of young Wistar rats. Pregnant rats were exposed to 10 mg of cadmium acetate per litre of drinking water, from initiation of pregnancy to parturition or until postnatal day 5. At birth or on postnatal day (PND) 5 the pups were weighed, sacrificed and brains were removed and frozen for later study. Protein, lipid and nucleic acid contents were measured and the brain Cd concentration was determined. Levels of dopamine (DA), 5-hydroxytryptamine (5-HT) and their respective metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) were measured in neonatal pup brain by higher performance liquid chromatography with electrochemical detection. The results from this experiment showed that Cd increased the 5-HT and 5-HIAA contents in all areas of the brain and the DA and DOPAC levels in mesencephalon, but decreased the DA and DOPAC levels in the metencephalon. On the other hand, Cd intoxication did not modify the other biochemical parameters measured, with the exception of a decrease in nucleic acids on PND 5.

Neurotoxic effects of gestational administration of low-dose lead acetate.

Lead acetate (300 mg l-1) was administered to pregnant Wister rats from day 1 of pregnancy to day 0 postpartum or day 5 postpartum, via drinking water. On these days, pups were sacrificed, collecting the blood to determine the concentration of lead by graphite furnace atomic absorption spectrophotometry. Brains were used to determine the total content of nucleic acids, DNA/RNA ratio and the total amount of proteins, lipids and monoamines. We found a reduction in protein content on day 0 postpartum, and changes in monoamine concentration on day 0 postpartum and day 5 postpartum. These data suggest that prenatal and early lactational exposure to a relatively low dose of lead could produce alterations in monoaminergic metabolism.

Testicular alterations in rats due to gestational and early lactational administration of lead.

A solution of lead acetate (300 mg/L) was administered via drinking water to pregnant Wistar rats from day 1 of pregnancy to delivery (Pb-treated day 0 group) or throughout gestation and early lactation (from day 1 to day 5 postnatal) (Pb-treated day 5 group). When the pups were born, four dams and their offspring in each group (control day 0, Pb-treated day 0, control day 5, and Pb-treated day 5) were sacrificed on day 0 (day 0 groups) or on day 5 (day 5 groups). Relative testicular weight and gross testicular structure were not altered by the treatment. The seminiferous tubule diameter and the number of prospermatogonia were reduced by the treatment. Determination of the n-ploidy stage of prospermatogonia indicates that these cells have more proliferative activity in Pb-treated rats than in control rats. On the other hand, the total DNA, RNA, and protein content of the testes in treated rats was significantly reduced, but the DNA: RNA ratio remained unaltered.

Seasonal changes in thyroid activity in male and female frog, Rana perezi.

Plasma T3 and T4 levels, and thyroid free (f) and bound (b) thyroid hormones contents, were determined by radioimmunoassay in adult male and female Rana perezi over 1 year. Plasma T3 levels show a significant seasonal cycle in both male and female frogs, increasing from January to peak in July (71-74 pg/ml) to decrease in August-October. Plasma T4 concentrations also varied seasonally, and sex differences were apparent. Basal T4 levels from the end of summer to the end of winter and higher values (682-651 pg/ml) in spring and early summer occur in female frogs; males have lowest levels in October (59.78 +/- 13.92 pg/ml) and higher levels during the rest of the year, except for a significant decrease in April. The thyroid content of fT3 and fT4 displayed similar seasonal patterns, with peak values in April and July-August. Sex differences are again present. The thyroid contents of bT3 are high between March and July in both sexes, with values in females being greater than those in males. The bT4 content follows a similar seasonal pattern in males and females and shows a minimum in March and a maximum in summer. Thyroid releasing capacity seems to change depending on the season and sex.

Corticotropin-releasing factor stimulates metamorphosis and increases thyroid hormone concentration in prometamorphic Rana perezi larvae.

Attempts to identify a hypothalamic molecule that stimulates thyrotropin (TSH) secretion from amphibian pituitary have been unsuccessful to date. The effects of mammalian (ovine and human) corticotropin-releasing factor (CRF) on the thyroid function of prometamorphic (Taylor & Kollros stages XI-XVII) (Taylor and Kollros, 1946) Rana perezi larvae were studied. Chronic treatments with both ovine and human CRF (oCRF, hCRF) stimulated metamorphosis while delaying larval growth. Chronic hCRF (1 microgram) administration induced 3.2- and 5.3-fold increases in whole body concentration of thyroxine (T4) and triiodothyronine (T3), respectively. In contrast, the 0.5-microgram dose of hCRF stimulated a significant (3.4-fold) increase in whole body concentration of T4 but not of T3. Histological studies of the thyroid gland revealed a 22% increase in the number of follicles per section as a result of the chronic treatment with oCRF (1 microgram). Acute oCRF (2 micrograms) treatment induced a significant increase in T4 concentration at 4 hr (1.3-fold) and 8 hr (2.3-fold) postinjection. T3 concentration was not altered. These results support previous reports and lead us to conclude that a CRF-like peptide, and not TRH, is involved in the regulation of thyroid activity in anuran amphibians during metamorphosis.

Morphine effects in brainstem-transected cats: I. EEG and 'sleep-wakefulness' in the isolated forebrain.

In order to examine the prosencephalic mechanisms that might sustain the effects of opiates on EEG and sleep-wakefulness, the actions of morphine sulfate on the EEG and the pupil size were examined in the chronically isolated forebrain of brainstem-transected cats. Single morphine doses (0.5, 2.0 or 3.0 mg/kg, i.p.) administered to these animals produced a long-lasting EEG desynchronization in the isolated forebrain which was associated with pupil mydriasis. The specificity of these morphine effects was shown by the fact that naloxone blocks both the EEG and pupillary effects of the drug. After morphine, spontaneous synchronized EEG with delta waves normally seen in the isolated forebrain preparation was suppressed for 6-18 h, followed by a strong rebound. Both the suppression and rebound in synchronization with delta waves occurred in a dose-dependent manner. The duration of these effects closely paralleled previously reported morphine effects on non-rapid eye movement (NREM) sleep in intact cats. Therefore, in relation to the effects of morphine on EEG and sleep-wakefulness in intact animals, this study suggests that: (1) Morphine suppression of NREM sleep and the subsequent arousal state of the animal are mediated by prosencephalic structures; (2) the generation of the typical neocortical EEG slow burst activity produced by opiates depends on lower brainstem structures.

Morphine effects in brainstem-transected cats: II. Behavior and sleep of the decerebrate cat.

Previous studies have shown that opiates suppress both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Furthermore, during the induced insomnia period, characteristic species-specific behaviors occur which are associated with high voltage slow waves in the EEG. This paper investigates the lower brainstem mechanisms involved in the generation of these effects, and describes the action of single morphine doses (0.5, 2.0 or 3.0 mg/kg, i.p.) on the behavior and REM sleep of chronic decerebrate cats. The effects of morphine in the decerebrate cat followed a 3-stage time course similar to that seen in intact cats: (1) autonomic manifestations (3-8 min postdrug); (2) a quiet state (10-60 min postdrug) with behavioral signs of NREM; and (3) a state of activated behavior (1-6 h postdrug), including motor activity and variations in muscle tone. The decerebrate cats also showed a dose-dependent suppression of REM sleep. The present results indicate that: (1) the lower brainstem provides the basic mechanisms for the behavioral deactivation-activation and the autonomic effects of the drug; (2) hypnogenic and synchronizing influences arising from the brainstem might induce the high voltage, slow burst EEG produced by opiates; (3) REM sleep suppression originates only partially in the lower brainstem; (4) the subsidiary action of the prosencephalon seems to be required for the full expression of the drug's effect on behavior and the EEG.