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PubMed1979

Carcinogenic effect of N-bis(2-hydroxypropyl)nitrosamine by a single administration in rats.

The carcinogenic effect of a single intraperitoneal injection of N-bis)2-hydroxypropyl)nitrosamine (BHP) was studied in male Wistar rats. Lung tumors (adenomas and adenocarcinomas) had the highest incidence (100%). Fewer neoplasms were induced in the thyroid (adenomas and adenocarcinomas, 36%), kidney (renal cell carcinomas, 8%), and the sigmoid colon (adenomas and adenocarcinomas, 9%). No pancreatic neoplasms were found.

Adenocarcinoma↗
PubMed1979

Identification of S-(carboxymethyl)-L-cysteine and thiodiglycolic acid, urinary metabolites of 2,2'-bis-(chloroethyl)-ether in the rat.

S-(carboxymethyl)-L-cysteine (CMC) and thiodiglycollic acid (TGA) were identified by gas chromatographic-mass spectrometric measurements in the urine of rats after intraperitoneal injections of 2,2'-bis-(chloroethyl)-ether (BCEE). It is therefore probable that BCEE is O-dealkylated by a mixed-function oxidation. The hepatocarcinogenic effect of BCEE may be explained by the liberation of chloroacetaldehyde in vivo.

Animals↗
PubMed1998

Oral versus intraperitoneal administration of irinotecan in the treatment of human neuroblastoma in nude mice.

The present study evaluated the plasma pharmacokinetics of irinotecan (CPT-11) and its effects against a human neuroblastoma in xenograft, given by different administration routes. One-third of the LD50 was administered either intraperitoneally (59 mg/kg mouse weight (MW)) or orally (404 mg/kg MW) to nude mice. The plasma levels of CPT-11 and its active metabolite SN-38 decreased rapidly when CPT-11 was administered intraperitoneally, but remained relatively high for 4-8 h after oral administration. Then, a human neuroblastoma xenograft was inoculated in another set of 21 nude mice. When the estimated tumor weight reached 150-200 mg, CPT-11 was administered in the total LD50 either intraperitoneally or orally in three doses at 4-day intervals (q4d x3) to the mice in each experimental group. Oral administration was found to be superior to intraperitoneal injection in terms of tumor inhibition and to be an effective route for CPT-11 administration in the treatment of human neuroblastoma in nude mice.

Administration, Oral↗
PubMed1999

Genotoxic effect of arecoline given either by the peritoneal or oral route in murine bone marrow cells and the influence of N-acetylcysteine.

The carcinogenic potentiality of the major alkaloid of betel nut, arecoline (ARC), is well established. This study was undertaken to determine the differences in genotoxic effects of ARC when given by two different routes (oral administration (OA) and intraperitoneal injection (IP)) in mouse bone marrow cells (BMC) since ARC carcinogenicity was observed only when ARC was given orally. The data indicate that ARC-OA induced a higher frequency of cancers, a greater delay in the cell cycle and greater sister chromatid exchanges than ARC-IP. The presence of N-acetyl cysteine along with ARC-OA significantly reduced the effect of ARC.

Acetylcysteine↗
PubMed1999

Assessment of aniline derivatives-induced DNA damage in the liver cells of B6C3F1 mice using the alkaline single cell gel electrophoresis ('comet') assay.

The alkaline single cell gel electrophoresis (SCGE) or 'comet' assay under alkaline conditions was used to measure DNA damage in the liver cells of B6C3F1 male mice exposed to 2,4-dimethylaniline and 2,4,6-trimethylaniline. Cells embedded in agarose were lysed, subjected briefly to an electric field, stained with a fluorescent DNA-binding stain, and viewed using a fluorescence microscope. The effect of 2,4-dimethylaniline and 2,4,6-trimethylaniline was studied after single intraperitoneal injections at doses equal to 100, 200 mg/kg and 150, 300 mg/kg body wt., respectively. It was found that 2,4-dimethylaniline and 2,4,6-trimethylaniline were able to damage DNA in the liver cells of the mice. As has been published elsewhere, the DNA damaging effect of the studied compounds was also observed in bone marrow cells of the mice. In conclusion, taking into account the results mentioned above and the results obtained by the other researchers who reported mutagenic activity of 2,4-dimethylaniline and 2,4,6-trimethylaniline in a Salmonella typhimurium assay and DNA repair test using Chinese hamster hepatocytes, it can be stated that both aromatic amines are genotoxic.

Aniline Compounds↗
PubMed2000

Assessment of allodynia and hyperalgesia after cisplatin administration to rats.

This work describes the behavioural responses of Sprague-Dawley rats to mechanical or thermal stimuli during and after administration of ten intraperitoneal injections of, alternatively, 1 and 2 mg/kg cisplatin every three days (cumulative dose: 15 mg/kg). Nociceptive signs including mechanical allodynia and hyperalgesia appeared after 3 and 6 cisplatin injections, respectively, and were maintained until 15 days after the last injection. The conservation of a good clinical status and fast appearance of symptoms are favourable criteria for using this animal model to understand the pathophysiological mechanisms implicated in the cisplatin-induced sensory peripheral neuropathy.

Animals↗
PubMed1997

In vivo expression of inducible nitric oxide synthase in supraventricular amoeboid microglial cells in neonatal BALB/c and athymic mice.

The present study investigated whether the supraventricular amoeboid microglial cells (SAMC) in neonatal BALB/c and athymic nude mice were able to express inducible nitric oxide synthase (iNOS) after intraperitoneal injections of lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma). The results showed that iNOS, undetectable in these cells in vehicle injected mice, could clearly be demonstrated immunohistochemically in a large number of them in LPS treated normal and mutant mice. Only a few iNOS-positive SAMC were observed in IFN-gamma injected mice. Immunoelectron microscopy confirmed the microglial nature of the labelled cells and that the immunoprecipitate of iNOS was cytosolic, being diffusely present throughout the cytoplasm of the cells. It is suggested that iNOS in the SAMC of neonatal BALB/c and athymic mice may be involved in the synthesis of nitric oxide which is necessitated more for host defence mechanism against bacterial endotoxin than against immunological stimuli.

Animals↗
PubMed1999

Expression and distribution of redox regulatory protein, thioredoxin after metabolic impairment by 3-nitropropionic acid in rat brain.

Thioredoxin (TRX) is a small, multifunctional protein with a redox-active site and multiple biological functions that include reducing activity for reactive oxygen intermediates. We assayed TRX by immunohistochemical methods in the rat brain after intraperitoneal injection of 3-nitropropionic acid (3-NP), an irreversible inhibitor of succinate dehydrogenase. Systemic administration of 3-NP produced lateral striatal, hippocampal CA1 and CA3 lesions in the present study. The immunoreactivity for TRX was enhanced in hippocampal CA3, dentate gyrus and lateral striatum, but not detected in hippocampal CA1 subfield after 3-NP intoxication. The data suggest that TRX may play an important role in the pathogenesis of 3-NP neurotoxicity.

Animals↗
PubMed2002

Attenuation of internal organ damages by exogenously administered epidermal growth factor (EGF) in burned rodents.

Major burns are associated with multiple internal organ damages, including necrosis of the gastrointestinal mucosa. Failure of the intestinal barrier is a serious complication in burned patients. Epidermal growth factor (EGF) is a mitogenic polypeptide that stimulates wound repair and affords protection to the gastric mucosa. We examined whether a single systemic intervention with EGF prevents organ systems damages, following full-thickness scalds (25-30%) in rodents. Animals were randomly assigned to receive an intraperitoneal injection of EGF (30 microg/kg in mice, 10 microg/kg in rats) or saline solution, 30 min prior thermal injury in mice or after the cutaneous injury in rats. General clinical condition and mortality during 24h were recorded. Animals were autopsied and histopathological and histomorphometric studies were conducted. Mice treated with EGF exhibited a milder clinical evolution and acute lethality was significantly reduced as compared to saline counterparts (P<0.01). Histopathological and morphometric analysis showed that EGF significantly reduced intestinal necrosis and contributed to preserve jejunoileal architecture in mice (P<0.05) and rats (P<0.01). The onset of renal hemorrhagic foci was significantly reduced in EGF-treated groups (P<0.01). Lung damages appeared attenuated in EGF-treated animals. These data indicate the salutary effects of EGF by attenuating internal complications associated to thermal injuries. Further studies are warranted to fully elucidate the usefulness of this therapy.

Animals↗
PubMed1997

Effects of systemic administration of 2-(4-phenyl-piperidino)-cyclohexanol (vesamicol) and an organophosphate DDVP on the cholinergic system in brain regions of rats.

Vesamicol is known to inhibit the transport of acetylcholine (ACh) into synaptic vesicles in vitro, but much less is known about its effects in the brain in vivo. To assess the effect of vesamicol in vivo, we examined cholinergic parameters, such as the subcellular distribution of ACh, activities of enzymes, uptake of choline, and muscarinic receptor binding in the striatum, hippocampus, and cerebral cortex of rats 30 and 60 min after intraperitoneal injection of vesamicol (3 mg/kg) or of vesamicol in combination with DDVP (5 mg/kg), which was administered 10 min before vasamicol. The levels of cytosolic ACh increased in all regions of the brain after injection of vesamicol, while those of vesicular ACh decreased in all regions except for the striatum. The increase in the levels of extracellular ACh and cytosolic ACh in the striatum induced by DDVP was generally enhanced after injection of vesamicol, Vesamicol did not reduce the level of vesicular ACh when DDVP had been injected previously. Vesamicol did not induce any significant changes in the activities of enzymes, choline uptake, or binding of [6H]quinuclidinyl benzilate to the muscarinic ACh receptors in the three regions. Changes in the cholinergic parameters caused by DDVP were not reversed by the combined administration of DDVP with vesamicol. The present results indicate that vesamicol can inhibit the transport of ACh into synaptic vesicles in the brain tissue in vivo, although it cannot reverse the effects of DDVP that has been injected prior to vesamicol.

Acetylcholine↗
PubMed2003

Effect of Indigofera aspalathoides against Dalton's ascitic lymphoma.

The effect of intraperitoneal injection of 400 mg/kg of ethanolic extract of Indigofera aspalathoides (EEIA) against Dalton's ascitic lymphoma has been evaluated in Swiss albino mice. A significant increase in the life span, a decrease in the cancer cell count and body weight were noted in the tumour-induced mice after treatment with EEIA. These observations indicate that the plant is having protective effect in Dalton's ascitic lymphoma.

Animals↗
PubMed2001

The effect of ferric-nitrilotriacetic acid on the profile of polyunsaturated fatty acids in the kidney and liver of rats.

Intraperitoneal injection of the iron-complex, ferric-nitrilotriacetate (Fe-NTA), induces renal proximal tubular damage associated with oxidative damage in vivo. Fe-NTA induced a time-dependent decrease of several polyunsaturated fatty acids (PUFA), together with increased conjugated diene values and decreased cellular levels of alpha-tocopherol and glutathione. At the time of maximum detectable oxidation (3 h), after the injection of a sublethal dose of Fe-NTA there were clear reductions in the peak values over the controls for several fatty acids notably, 20:5 (eicosapentaenoic acid) (36%), 22:6 (docosahexanoic acid) (30%), 20:3 n6 (eicosatrienoic acid) (30%) and 20:4 (arachidonic acid) (28%) in the kidney. Fewer fatty acids showed a reduction in their residual values in the liver. 20:5 was reduced by 45% and for the 18:3 n3 and 18:3 n6, reductions of 35%, respectively. The profile of PUFAs is sensitive to the oxidative damage due to Fe-NTA and this may find applications as oxidative biomarker model.

Animals↗
PubMed2002

Behavioural assessment of dimethylsulfoxide neurotoxicity in rats.

Dimethylsulfoxide (DMSO) is a solvent used to dissolve hydrophobic drugs. Recent studies have demonstrated that repeated administration of DMSO induces significant disorders of the peripheral nervous system. To address this issue, we have studied the behavioural effects of repeated intraperitoneal injections of various concentrations of DMSO (1.8-3.6-7.2%) in male Sprague-Dawley rats. Behavioural effects were assessed with a commonly used battery of sensory and motor tests. The motor tests used were actimeter and grip strength test. Sensory test used noxious and non-noxious mechanical (paw pressure test and von Frey hairs test) and thermal (plantar test and tail immersion test) stimuli. Clinical status of the animals was good throughout the experiment and no motor deficits were observed. Nevertheless, sensory assessment displayed a mechanical allodynia of short duration.

Animals↗
PubMed2003

Effect of alpha-ketoglutarate and oxaloacetate on brain mitochondrial DNA damage and seizures induced by kainic acid in mice.

The effects of alpha-ketoglutarate and oxaloacetate on brain mitochondrial DNA (mtDNA) damage and seizures induced by kainic acid were examined both in vivo and in vitro. An intraperitoneal (ip) injection of kainic acid (45 mg/kg) produced broad-spectrum limbic and severe sustained seizures in all of the treated mice. The seizures were abolished when alpha-ketoglutarate (2 g/kg) or oxaloacetate (1 g/kg) was injected intraperitoneally in the animals 1 min before kainic acid administration. In addition, the administration of kainic acid caused damage to mtDNA in brain frontal and middle cortex of mice. These effects were completely abolished by the ip preinjection of alpha-ketoglutarate (2 g/kg) or oxaloacetate (1 g/kg). In vitro exposure of kainic acid (0.25, 0.5 or 1.0 mM) to brain homogenate inflicted damage to mtDNA in a concentration-dependent manner. The damage of mtDNA induced by 1.0 mM kainic acid was attenuated by the co-treatment with alpha-ketoglutarate (2.5 or 5.0 mM) or oxaloacetate (0.75 or 1.0 mM). Furthermore, in vivo and in vitro exposure of kainic acid elicited an increase in lipid peroxidation. However, the increased lipid peroxidation was completely inhibited by cotreatment of alpha-ketoglutarate or oxaloacetate. These results suggest that alpha-keto acids such as alpha-ketoglutarate and oxaloacetate play a role in the inhibition of seizures and subsequent mtDNA damage induced by the excitotoxic/neurotoxic agent, kainic acid.

Animals↗
PubMed1997

Effect of dietary iron-deficiency on the disposition of nickel in rats.

Nickel was given orally to iron-deficient and iron-sufficient rats and the levels of the metal in various tissues were examined at several time intervals. The results showed higher levels of nickel in the tissues of the iron-deficient rats, as compared to the iron-sufficient ones, 3, 6, 24, 48 and 120 h following gastric intubation of the metal. The results also showed higher levels of the metal in some tissues of iron-deficient rats than in iron-sufficient ones 24 h after intra-peritoneal nickel administration. A lower urinary excretion of nickel was observed in the iron-deficient rats given the intraperitoneal injections, as compared to the iron-sufficient animals. Our results indicate that nickel, at least in part, is taken up by the absorptive mechanism for iron in the intestinal epithelium. In addition, the iron-status appears to affect the uptake of nickel from the blood into the tissues.

Administration, Oral↗
PubMed1997

A highly toxic PCB produces unusual changes in the fatty acid composition of rat liver.

The changes in lipid metabolism produced by a coplanar PCB were studied in rats. Male Wistar rats were given a single intraperitoneal injection of 3,3',4,4',5-pentachlorobiphenyl at a dose of 25 mg/kg. After 5 days of administration, total hepatic lipids were treated with 1 M KOH in methanol at 75 degrees C and the liberated fatty acids were analyzed by HPLC after conversion to fluorescent derivatives. In comparison with free-fed and pair-fed control groups, the proportion of arachidonic acid in the PenCB-treated rats was reduced by about 50%, while oleic and linoleic acids increased significantly. We also examined the individual glycerophospholipids, separated by TLC, to see if they were affected by alteration in the fatty acid composition of the whole liver. In all glycerophospholipids, the proportion of arachidonic acid was reduced significantly to the same degree while linoleic acid increased. Changes in the activity of desaturase isozymes have been postulated to explain this unusual lipid metabolism following administration of a toxic PCB and this may contribute to its toxicity.

Animals↗
PubMed2000

Retrospective evaluation of serum ornithine carbamyltransferase activity as an index of hepatotoxicity in toxicological studies with rats.

The sensitivity of elevated serum ornithine carbamyltransferase (OCT) as an index of hepatotoxicity in rats was assessed in different studies conducted over a number of years and originally designed to examine the toxicity or carcinogenicity of a variety of test chemicals and diets. Changes in serum OCT activities were compared with the more widely used clinical endpoints, alanine aminotranserase (ALT) and aspartate aminotransferase (AST). In the first study, rats received a single oral dose of the hepatotoxic and hepatocarcinogenic fungal toxin aflatoxin B(1) (AFB(1)). The increase in enzyme levels between control and AFB(1)-treated rats was greater for serum OCT than for ALT or AST. This response was similar to the changes in serum enzyme levels in studies where rats ingested a hepatotoxic and hepatocarcinogenic choline deficient (CD) diet. When rats were exposed to the hepatotoxic and nephrotoxic fungal toxin fumonisin B(1) (FB(1)) by intraperitoneal injection for 6 days, serum AST and ALT were significantly elevated above control levels while OCT was unaffected. The peroxisome proliferator ciprofibrate caused elevated ALT and AST but not OCT at week 52 of dietary exposure, after the development of liver nodules and tumours. Of the two liver-specific enzymes examined in all of the studies, ALT was more consistently predictive of hepatotoxicity than OCT.

Administration, Oral↗
PubMed2003

Effects of alpha-tocopherol on noise-induced hearing loss in guinea pigs.

Preventing noise-induced hearing loss (NIHL) by antioxidants is based on the hypothesis that generation of reactive oxygen species is one of the causes of NIHL. alpha-Tocopherol is a naturally occurring antioxidant with no noticeable side effects. In this study, we attempted to protect guinea pigs from developing NIHL by administering alpha-tocopherol. Pigmented male guinea pigs were exposed to a noise (4 kHz octave band, 100 dB SPL), 8 h/day for 3 days consecutively. alpha-Tocopherol (10 mg/kg or 50 mg/kg daily) was given by intraperitoneal injection from 3 days before through 3 days after the noise exposure. Auditory evoked brainstem response (ABR) thresholds at 2, 4 and 8 kHz were recorded prior to the experiment, immediately post-noise, 2 and 8 days post-noise. On day 8 post-noise, after the ABR recording, guinea pigs were decapitated and the cochleae were removed for cochlear surface preparations and scanning electron microscope (SEM) study. ABR threshold shifts of groups receiving alpha-tocopherol were significantly smaller than those of groups not receiving alpha-tocopherol at all frequencies and all time points tested except that of group 3 at 8 kHz 8 days post-noise. No hair cell loss was seen on the surface preparations, but stereocilia loss was found by SEM study. The noise-induced stereocilia loss was significantly decreased by alpha-tocopherol. These results indicate that alpha-tocopherol can attenuate the noise-induced cochlear damage. Further investigations on the preventive effect of alpha-tocopherol on NIHL in noise-exposed workers are necessary.

Animals↗