Dominant lethal study ofSpirulina maxima in male and female rats after short-term feeding

1996 ◽  
Vol 10 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Gérman Chamorro ◽  
María Salazar ◽  
Nicole Pages
2021 ◽  
pp. 074823372110105
Author(s):  
Roberta Tassinari ◽  
Andrea Martinelli ◽  
Mauro Valeri ◽  
Francesca Maranghi

Synthetic amorphous silica (SAS) nanomaterial – consisting of aggregates and agglomerates of primary silicon dioxide (SiO2) particles in the nanorange (<100 nm) – is commonly used as excipient in pharmaceuticals, in cosmetics and as food additive (E551). The available data suggest that SAS nanoparticles (NP) after intravenous (IV) exposure persist in liver and spleen; however, insufficient data exist to verify whether SAS may also induce adverse effects. The aim of the present study was to verify the potential long-term effects of SAS NP (NM-203) on spleen and liver as target organs following short-term exposure. Adult male and female Sprague-Dawley rats were treated by IV injection in the tail vein with a single (1-day) dose (SD) and repeated (5-day) doses (RD) of 20 mg/kg bw per day of SAS dispersed in sterile saline solution as vehicle. Histopathological examinations of target organs were performed after 90 days. Tissue biodistribution and full characterization of NM-203, primary particle size 13–45 nm, was performed within the framework of the Nanogenotox project. No mortality or general toxicity occurred; histopathological analysis showed splenomegaly in the RD group accompanied by inflammatory granulomas in both sexes. Granulomas were also present in liver parenchyma in the RD (both sexes) and SD groups (male only). The histopathological results indicated that SAS NP have the potential to persist and induce sex-specific chronic inflammatory lesions in spleen and liver upon short-term treatment. Overall, the data showed that the widespread use of silica in drugs might elicit chronic reactions in spleen and liver prompting to the need of further investigations on the safety of SAS NP.


Author(s):  
Xiaomeng Qiao ◽  
Mizhu Sun ◽  
Yuanyuan Chen ◽  
Wenyang Jin ◽  
Huan Zhao ◽  
...  

Abstract Aims Ethanol ingestion affects cognition and emotion, which have been attributed to the dysfunction of specific brain structures. Studies of alcoholic patients and animal models consistently identify reduced hippocampal mass as a key ethanol-induced brain adaptation. This study evaluated how neuroadaptation in the hippocampus (Hip) produced by ethanol contributed to related behavioral deficits in male and female rats. Methods Effects of acute, short-term and long-term ethanol exposure on the anxiety-like behavior and recognition memory on adult male and female Sprague–Dawley rats were assessed using elevated plus maze test and novel object recognition test, respectively. In addition, in order to investigate the direct effect of ethanol on hippocampal neurons, primary culture of hippocampal neurons was exposed to ethanol (10, 30 and 90 mM; 1, 24 and 48 h), and viability (CCK-8) and morphology (immunocytochemistry) were analyzed at structural levels. Western blot assays were used to assess protein levels of NT3-TrkC-ERK. Results Acute and short-term ethanol exposure exerted anxiolytic effects, whereas long-term ethanol exposure induced anxiogenic responses in both sexes. Short-term ethanol exposure impaired spatial memory only in female rats, whereas long-term ethanol exposure impaired spatial and recognition memory in both sexes. These behavioral impairments and ethanol-induced loss of hippocampal neurons and decreased cell viability were accompanied by downregulated NT3-TrkC-ERK pathway. Conclusion These results indicate that NT3-TrkC-ERK signaling in the Hip may play an important role in ethanol-induced structural and behavioral impairments.


1988 ◽  
Vol 7 (5) ◽  
pp. 675-685 ◽  
Author(s):  
J.F. Borzelleca ◽  
L.W. Condie ◽  
J.L. Egle

To assess adverse effects that might be caused by an event resulting in high levels of barium in drinking water, rats were gavaged with barium chloride (BaCl2 at dosage levels of 30, 100, and 300 mg/kg in a 1-day study and at 100, 145, 209, and 300 mg/kg for 10 days, and the effects were determined. LD50 values for male and female rats were found to be 419 (352–499) and 408 (342–487) mg/kg BaCl2, respectively. In the 1-day exposure study, decreases in body weight and liver/brain weight ratios and increase in kidney weight as a percentage of body weight appeared to be related to barium ingestion at 300 mg/kg. After 10 days of exposure to barium, survival of females was substantially lower at 300 mg/kg. A reduction in ovaries/brain ratio at 300 mg/kg appeared to be barium-induced. There was a decrease in BUN at 300 mg/kg in males and at all dose levels in females. No other effects were attributed to barium. Histopathological findings were negative in both the 1-and 10-day studies. It is concluded that short-term oral exposure to BaCl2 at doses up to 209 mg/kg produces no significant adverse health effects.


1978 ◽  
Vol 56 (5) ◽  
pp. 747-753 ◽  
Author(s):  
Edwin A. Knecht ◽  
Gary L. Wright ◽  
Mark A. Toraason

Reproductive function of male and female rats was examined in relation to periodic, short-term heat treatment. Daily exposure to an environmental temperature of 38.2 °C for 55 min elevated rectal temperatures to 39.9 and 41.2 °C in male and female rats, respectively. Heat exposure tended to decrease copulation in males cohabitated with unhealed females. The rate of conception was affected similarly, and fetal survival tended to be reduced by paternal heat treatment. Estrous cycles were disrupted initially in heat-exposed females, but the rate of copulation and conception of females cohabitated with unheated males was unaltered by heat treatment. However, maternal heat exposure impaired prenatal survival and growth. During lactation, a high incidence of maternal and pup deaths was observed at approximately 14 days postpartum. Maternal deaths were coincident with a decrease in thermoregulatory ability and rectal temperatures exceeding 42 °C.


1993 ◽  
Vol 75 (3) ◽  
pp. 1140-1149 ◽  
Author(s):  
D. J. Prezant ◽  
D. E. Valentine ◽  
E. I. Gentry ◽  
B. Richner ◽  
J. Cahill ◽  
...  

The effects of short-term (2.5 wk) and long-term (10 wk) testosterone propionate (2.5 mg/day; 5 days/wk) treatment on diaphragm contractility, fatigue resistance, and fiber type proportions were studied in male and female rats. Contractility and fatigue resistance indexes were measured in an in vitro diaphragm costal strip preparation by direct stimulation at 37 degrees C. The fatigue paradigm consisted of 30 trains/min at 5 Hz (50% duty cycle) for 10 min. Fatigue resistance indexes were calculated as postfatigue divided by baseline forces. In females but not males, testosterone treatment produced significant increases in body weight, costal diaphragm weight, and contractility and significant decreases in fatigue resistance indexes. The interaction between testosterone treatment and the duration of treatment was significant, with the increase in contractility (females) being significant after short-term but not long-term treatment. No significant difference in fiber type proportions or areas was observed, regardless of treatment duration or the preexperimental, basal circulating level of androgen.


1993 ◽  
Vol 13 (5) ◽  
pp. 359-368 ◽  
Author(s):  
L. B. Sasser ◽  
J. A. Cushing ◽  
J. C. Dacre

1996 ◽  
Vol 150 (2) ◽  
pp. 169-178 ◽  
Author(s):  
G A C van Haasteren ◽  
E Linkels ◽  
H van Toor ◽  
W Klootwijk ◽  
E Kaptein ◽  
...  

Abstract The reduced thyroid activity during short-term starvation is associated with a lowered hypothalamic synthesis and secretion of TRH. However, little is known about the cause of the reduced thyroid function during prolonged malnutrition. We have therefore studied the effects of food reduction to one-third of normal (FR33) on the hypothalamus-pituitary-thyroid axis of male and female Wistar rats. After 3 weeks body weights of FR33 rats were almost 50% lower than those of controls. In both sexes, FR33 caused marked increases in serum corticosterone, and decreases in serum TSH, thyroxine (T4), free T4, tri-iodothyronine (T3) and free T3. While the free T3 fraction (FFT3) in serum decreased, the free T4 fraction (FFT4) tended to increase. Electrophoretic analysis indicated that decreased FFT3 was correlated with an increased thyroxine-binding globulin, while the increase in FFT4 seemed due to a decreased thyroxine-binding prealbumin binding capacity. Total RNA and proTRH mRNA in the hypothalamus were not affected by FR33. Median eminence and posterior pituitary TRH content tended to increase in FR33 rats, suggesting that hypothalamic TRH release is reduced in FR33 rats. Anterior pituitary TSH content was decreased by FR33 in both sexes, but pituitary TSHβ mRNA and TRH receptor status were not affected except for increased pituitary TSHβ mRNA in female FR33 rats. Although FR33 had no effect on pituitary weight, pituitary RNA and membrane protein content in FR33 rats were 50–70% lower than values in controls. In conclusion, prolonged food reduction suppresses the pituitary-thyroid axis in rats. In contrast to short-term food deprivation, the mechanism whereby serum TSH is suppressed does not appear to involve decreases in proTRH gene expression, but may include effects on pituitary mRNA translation. Our results further support the hypothesis that TSH release may be lowered by increased corticosterone secretion, although the mechanism of this effect may differ between acute starvation and prolonged food reduction. Journal of Endocrinology (1996) 150, 169–178


1986 ◽  
Vol 110 (2) ◽  
pp. 367-373 ◽  
Author(s):  
N. G. Weiland ◽  
C. A. Barraclough ◽  
K. J. Catt

ABSTRACT Considerable differences have previously been found in the hypothalamo-hypophysial responsiveness to oestrogen, depending upon the time between gonad removal and exposure to oestrogen. In the present study a detailed analysis was made of some of the differences which may exist in pituitary LH-releasing hormone (LHRH) receptors and the amount of LH released in response to electrochemical depolarization of the medial preoptic area after 2 or 7 days of oestradiol treatment of long- and short-term gonadectomized male and female rats. The pituitary glands of long-term gonadectomized males and females secreted more LH in response to two pulse injections of LHRH than did short-term gonadectomized rats. The amount of LH released on day 2, however, was equivalent to that secreted after 7 days of oestradiol treatment. Moreover, long-term gonadectomized males and females had equivalent LHRH receptor concentrations, which were greater than those of short-term gonadectomized animals. Peak serum LH concentrations observed after preoptic stimulation were equivalent in short- and long-term castrated rats after 2 days of oestrogen exposure. Serum LH concentrations following preoptic stimulation in short-term gonadectomized males and females were significantly greater on day 7 than on day 2 of oestradiol treatment, whereas in long-term gonadectomized animals the stimulated release of LH was equivalent both in magnitude and time of peak release on both days. These studies demonstrate that the differential effects of oestradiol on LH release on day 2 (no negative feedback) compared with day 7 (both negative and positive feedback exist) are not due to differences in the ability of the pituitary gland to release LH in response to LHRH, nor in the releasable pools of hypothalamic LHRH in long-term gonadectomized rats. Rather, they seem to be due to a refractoriness in some unidentified central nervous process which regulates tonic LH release in gonadectomized rats. J. Endocr. (1986) 110, 367–373


2020 ◽  
pp. 803-812
Author(s):  
S SEELEY ◽  
M D’SOUZA ◽  
T STOOPS ◽  
B RORABAUGH

Methylphenidate is commonly used for the treatment of attention deficit hyperactivity disorder. The cardiovascular safety of methylphenidate has been a subject of debate with some studies indicating that methylphenidate increases the likelihood of experiencing a myocardial infarction. However, it is unknown whether methylphenidate worsens the extent of injury during an ischemic insult. The purpose of this study was to determine whether short term exposure to methylphenidate increases the extent of myocardial injury during an ischemic insult. Male and female rats received methylphenidate (5 mg/kg/day) or saline for 10 days by oral gavage. Hearts were subjected to 20 min of ischemia and 2 h of reperfusion on a Langendorff isolated heart apparatus on day 11. Cardiac contractile function was monitored via an intraventricular balloon and myocardial injury was assessed by triphenyltetrazolium chloride staining. Methylpheni-date significantly increased locomotor activity in male and female rats, confirming absorption of this psychostimulant into the central nervous system. Male hearts had significantly larger infarcts than female hearts, but methylphenidate had no impact on infarct size or postischemic recovery of contractile function in hearts of either sex. These data indicate that methylphenidate does not increase the extent of injury induced by an ischemic insult.


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