Toxic effects of chromium (VI) by maternal ingestion on liver function of female rats and their suckling pups (original) (raw)

THE OUTCOMES OF POTASSIUM DICHROMATE INTAKE IN SUCKLING PERIOD ON REPRODUCTIVE BIOMARKER OF EXPOSURE

Hexavalent chromium compounds occur mostly due to anthropogenic origin and are known to cause in humans and experimental animals hepatotoxicity, nephrotoxicity. The aim of this study was the evaluation of reproductive chromium toxicity, respectively exposure impact on biomarker of exposure: chromium level in genital organs and sexual accessory glands. Female rats, divided in four groups: three experimental and one control, were exposed via drinking water to potassium dichromate after delivery as follows: E 1-25 ppm Cr VI (LOAEL); E 2-50 ppm Cr VI; E3-75 ppm Cr VI, control received tap water without chromium content. The pups from each E group were exposed via milk and drinking water. After weaning and until sexual maturity pups received only tap water without chromium. The study pointed out: significant increase of chromium concentration in testis, epididymis, seminal vesicles, prostate and bulbo-urethral glands in all exposed groups comparative to control ones, and directly correlated to exposure level.

Chromium induced teratogenicity in female rat

Toxicology Letters, 1996

Exposure to chromium (VI) (250, 500 and 750 ppm as potassium dichromate) via drinking water pregestationally in rats revealed embryo-and fetotoxic effects in the form of a significant reduction in the number of implantations and number of fetuses. An increase in the number of resorptions, pre-implantation and post-implantation loss in chromium (VI)-treated mothers was also observed. No significant visceral abnormality was found. A significant increase in sub-dermal hemorrhagic patches on thoracic and abdominal areas was found. Skeletal abnormality in the form of reduced ossification in parietal, interparietal and caudal bones was found in the fetuses of chromium (VI)-treated mothers. Chromium levels in blood, placenta and fetuses were found to be significantly increased in the 500 ppm and 750 ppm dosed groups. The duration of estrus cycle was significantly altered after chromium (VI) exposure. This study suggests that chromium exposure in rat causes a lower degree of toxicity than in mice as observed in our earlier studies.

GLUTATHIONE DYNAMICS IN THE SECOND GENERATION YOUNG RATS BLOOD AS A CONSEQUENCE OF FEMALE EXPOSURE TO Cr(VI) INTOXICATION DURING GESTATION

2009

Chromium compounds are found in the environment, due to erosion of chromium containing rocks and can be distributed by volcanic eruptions in food, water. Metals being non-biodegradable persist in the environment for a long period and cause serious ecotoxicological problems. Chromium, which exists in nature mostly in the trivalent form (Cr +3 ), is essential for activating certain enzymes and for stabilizing proteins and nucleic acids. We have studied the influence of the glutathione dynamics in the second generation rats blood, as a consequence of females chromium (VI) intoxication during the gestation. This study was carried out on 7 Wistar adult female rats, control group (C), 21 adult Wistar female rats, devided in three experimental groups (E) and theire young rats. The rats were feet, durind the gestation, with 25ppm (LOAEL), 50ppm and 75ppm potassium dichromate, ad libitum, in drinking water. The control batch received tap water. Reduced glutathione (GSH) was measured quantita...

Haematological study in hexavalent chromium toxicity in female wistar rats and its progeny

The Pharma Innovation Journal, 2018

An experiment was conducted to study the haematological profile in 120 female wistar rats in chromium toxicity. Rats were provided with feed and water ad libitum. The duration of experiment was for four months. There were six groups where as group I was the control group. Group II was provided with potassium dichromate @ 500ppm in drinking water orally for three months along with the basal diet, group III was treated as Vitamin C control, group IV as Emblica officinalis control, group V and VI were protective and ameliorative groups. The haematological profile revealed a significant (p<0.05) reduction of haemoglobin (Hb), packed cell volume (PCV), total erythrocyte count (TEC) and total leukocyte count (TLC) in toxin group. Group V and VI recorded mild to moderate results indicating the protection offered by ameliorating agents used in the feed (Vitamin C @100 mg/kg body weight and Emblica officinalis@ 2%).

Oxidative stress, DNA damage, and antioxidant enzyme activity induced by hexavalent chromium in Sprague-Dawley rats

Environmental Toxicology, 2009

Chromium is a widespread industrial compound. The soluble hexavalent chromium Cr (VI) is an environmental contaminant widely recognized as carcinogen, mutagen, and teratogen toward humans and animals. The fate of chromium in the environment is dependent on its oxidation state. The reduction of Cr (VI) to Cr (III) results in the formation of reactive intermediates leading to oxidative tissue damage and cellular injury. In the present investigation, Potassium dichromate was given intraperitoneally to Sprague-Dawley rats for 5 days with the doses of 2.5, 5.0, 7.5, and 10 mg/kg body weight per day. Oxidative stress including the level of reactive oxygen species (ROS), the extent of lipid peroxidation and the activity of antioxidant enzymes in both liver and kidney was determined. DNA damage in peripheral blood lymphocytes was determined by single-cell gel electrophoresis (comet assay). The results indicated that administration of Cr (VI) had caused a significant increase of ROS level in both liver and kidney after 5 days of exposure, accompanied with a dose-dependent increase in superoxide dismutase and catalase activities. The malondialdehyde content in liver and kidney was elevated as compared with the control animals. Dose-and time-dependent effects were observed on DNA damage after 24, 48, 72, and 96 h posttreatment. The results obtained from the present study showed that Cr (VI) could induce dose-and time-dependent effects on DNA damage, both liver and kidney show defense against chromium-induced oxidative stress by enhancing their antioxidant enzyme activity. However, liver was found to exhibit more antioxidant defense than the kidney.

www.mdpi.com/journal/ijerph Article Potassium Dichromate Induced Cytotoxicity, Genotoxicity and Oxidative Stress in Human Liver Carcinoma (HepG2) Cells

2015

Abstract: Chromium is a widespread industrial waste. The soluble hexavalent chromium Cr (VI) is an environmental contaminant widely recognized to act as a carcinogen, mutagen and teratogen towards humans and animals. The fate of chromium in the environment is dependent on its oxidation state. Hexavalent chromium primarily enters the cells and undergoes metabolic reduction to trivalent chromium, resulting in the formation of reactive oxygen species together with oxidative tissue damage and a cascade of cellular events. However, the results from in vitro studies are often conflicting. The aim of this study was to develop a model to establish relationships between cytotoxicity, genotoxicity and oxidative stress, in human liver carcinoma [HepG2] cells exposed to potassium dichromate. HepG2 cells were cultured following standard protocols and exposed to various concentrations [0-50 µM] of potassium dichromate [K2Cr2O7]. Following exposure to the toxic metal, the MTT assay was performed t...

Embryo and fetotoxicity of hexavalent chromium: a long-term study

Toxicology Letters, 1998

Ingestion of chromium(VI) (250, 500 or 750 ppm as potassium dichromate, K 2 Cr 2 O 7) through drinking water by female rats for 3 months prior to gestation was toxic to embryo and fetus. There was a significant reduction in number of implantations and number of fetuses and an increase in number of resorptions and pre-implantation and post-implantation losses. No significant visceral abnormality was found. The increase in the number of subdermal hemorrhagic patches on the thorax and abdomen was significant. Skeletal abnormality in the form of reduced ossification in parietal, interparietal and caudal bones was observed in fetuses. Chromium levels in the blood of mothers, placenta and fetuses showed a significant increase. Duration of the estrous cycle was also increased significantly. The study revealed that long-term chromium exposure in rats did not cause embryo and fetotoxicity in a duration-dependent manner compared to short-term treatment as observed earlier. A possible explanation could be that, in the 90-day study, the female rats did not mate for three estrous cycles, thus giving time for clearance of a sizable amount of chromium from their bodies.

Study on Effects of Chromium on Antioxidant Enzymes in Mice

International Research Journal of Pharmacy, 2019

Chromium, naturally occurring, largest environmental toxicant that affects human health and most common pollutant; over the last few decades, it has been a concern that the fresh water consisting of massive metals can be agitated because of their campaigns primarily through the fraudulent programs of humans, industrial and domestic programs, chromium, heavy metal, primarily in oxidation states of hexavalent. Chromium obstructs the metabolic pathways and despite of all the above Chromium is an essential nutrient. Chromium adverse effects at low level is not well established. Hence, the study intended to examine the alterations of chronic exposure to chromium at low dose on antioxidant defense enzymes in mice. Exposure to chromium depleted significantly in catalyses, superoxide dismutase, and GST activity (p < 0.0001) in brain, liver and kidney when compared with their respective control group. The catalyses are considered one of the most important free radical scavenging enzymes, and the body's secondary protection against oxygen metabolites produced by the transformational massive metals increased activity levels of CAT, GST and SOD formation was observed experimental animals. The increase in antioxidant enzymes in Cr-treated animals indicated that one of the Cr-induced toxic effects as generated free radicals and in turn damages cell membrane.

Chromium-induced excretion of urinary lipid metabolites, DNA damage, nitric oxide production, and generation of reactive oxygen species in Sprague-Dawley rats

Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, 1995

Chromium and its salts induce cytotoxicity and mutagenesis, and vitamin E has been reported to attenuate chromate-induced cytotoxicity. These observations suggest that chromium produces reactive oxygen species which may mediate many of the untoward effects of chromium. We have therefore examined and compared the effects of Cr(III) (chromium chloride hexahydrate) and Cr(VI) (sodium dichromate) following single oral doses (0.50 ld50) on the production of reactive oxygen species by peritoneal macrophages, and hepatic mitochondria and microsomes in rats. The effects of Cr(III) and Cr(VI) on hepatic mitochondrial and microsomal lipid peroxidation and enhanced excretion of urinary lipid metabolites as well as the incidence of hepatic nuclear DNA damage and nitric oxide (NO) production were also examined. Increases in lipid peroxidation of 1.8- and 2.2-fold occurred in hepatic mitochondria and microsomes, respectively, 48 hr after the oral administration of 25 mg Cr(VI)/kg, while increases of 1.2- and 1.4-fold, respectively, were observed after 895 mg Cr(III)/kg. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT) and acetone (ACON) were determined at 0–96 hr after Cr administration. Between 48 and 72 hr post-treatment, maximal excretion of the four urinary lipid metabolites was observed with increases of 1.5- to 5.4-fold in Cr(VI) treated rats. Peritoneal macrophages from Cr(VI) treated animals 48 hr after treatment resulted in 1.4- and 3.6-fold increases in chemiluminescence and iodonitrotetrazolium reduction, indicating enhanced production of Superoxide anion, while macrophages from Cr(III) treated animals showed negligible increases. Increases in DNA single strand breaks of 1.7-fold and 1.5-fold were observed following administration of Cr(VI) and Cr(III), respectively, at 48 hr post-treatment. Enhanced production of NO by peritoneal exudate cells (primarily macrophages) was monitored following Cr(VI) administration at both 24 and 48 hr post-treatment with enhanced production of NO being observed at both timepoints. The results indicate that both Cr(VI) and Cr(III) induce an oxidative stress at equitoxic doses, while Cr(VI) induces greater oxidative stress in rats as compared with Cr(III) treated animals.

Effect of potassium dichromate intake on water consumption and toxic amount intake, in female rats, Rattus norvegicus (exposure on three generations)

2010

Material and methods: The study was carried out on three generations of female rats, each generation comprising 28 white Wistar adult female rats, divided in three experimental (E) groups, exposed to 25 ppm Cr – LOAEL (E1), 50 ppm Cr (E2), 75 ppm Cr (E3) and one control (C) group tap water. Results: It pointed out significant decrease of water daily mean consumption in experimental groups comparative to C group, inversely, significantly correlated with the exposure level, in F0, F1 and F2 generations, the mean daily water intake decreasing with the increase of the number of generations exposed, the lowest being found in the case of F2 generation, followed by F1 generation and F0, the differences being insignificant. Also hexavalent chromium intake was calculated, F2 generation having the poorest appetite for water, received the smallest amount of toxic, but yet not undermining the gravity of exposure in F2 generation, due to parental exposure factors.