Palm oil extracts protected against cadmium chloride poisoning via inhibition of oxidative stress in rats

Background The probable mechanism of an earlier reported capacity of palm oil extracts to confer protection against high dose cadmium poisoning in rats was reported in this study. Similar experimental design earlier reported by us was retained. Rats therefore were sacrificed at intervals of twelve; twenty four and forty eight hours post CdCl2 insult. Results Oxidative stress and antioxidant status (malondialdehyde, superoxide dismutase, catalase and glutathione) were assessed in tissues (liver, kidney, heart, brain, muscle) and serum. Oxidative stress indicators showed a significantly (p < 0.05) increased lipid peroxidation and alterations in antioxidant defence systems occasioned by drop in catalase and superoxide dismutase enzymes (serum, liver, heart, brain and kidneys) of the rats. Also observed were significant (p < 0.05) reduction in the non-enzymatic antioxidant reduced glutathione over time. Pre-administration of rats with the crude palm oil and its extracts modulated cadmium mediated depletion of the antioxidant capacities of rats acutely exposed to cadmium and rising lipid peroxidation profile. Conclusions Regulation of stress and antioxidant response was the underlying mechanism by which the extracts conferred protection against high dose cadmium insult thus suggesting its potential as a viable therapeutic target against its deleterious effects. Graphical Abstract

A Review on the Effects of Cadmium Toxicity on Living Beings

Cadmium is a toxic transition heavy metal with perilous effects on the health of animals and humans by indefinite ways. It is one of the asserted carcinogens group given by IARC. There are jillion ways by which cadmium may be prevalent in the environment as the pollutant or may be through contaminated water, food or by smoking. Cadmium poisoning may be seen in the form of itai itai disease. It came in knowledge after its outbreak in Japan in 1960s after the consumption of cadmium-contaminated rice as a food source. The exposure and accumulation of cadmium may lead to numerous forms of cancer, including breast, lung, prostate and nasopharynx, pancreas and kidney cancers. It expresses its effect by formation of stress proteins that depends on the amount of exposure and time of exposure. It had shown effects on the functioning of mitochondria resulting in formation of less energy or ATP (adenosine triphosphate) and more ROS. Other effects are cell apoptosis and inhibit growth, division and carcinogenic activity in cells. The current study has been done to understand the various effects scrutinised by numerous workers.

Palm oil extracts’ protected against cadmium chloride poisoning via inhibition of oxidative stress in rats”

Background: The probable mechanism of an earlier reported capacity of palm oil extracts to confer protection against high dose cadmium poisoning in rats was reported in this study. Similar experimental design earlier reported by us was retained. Rats therefore were sacrificed at intervals of twelve; twenty four and forty eight hours post CdCl2 insult. Results: Oxidative stress and antioxidant status (malondialdehyde, superoxide dismutase, catalase and glutathione) were assessed in tissues (liver, kidney, heart, brain, muscle) and serum. Oxidative stress indicators showed a significantly (p<0.05) increased lipid peroxidation and alterations in antioxidant defence systems occasioned by drop in catalase and superoxide dismutase enzymes (serum, liver, heart, brain and kidneys) of the rats. Also observed were significant (p<0.05) reduction in the non-enzymatic antioxidant reduced glutathione over time. Pre-administration of rats with the crude palm oil and its extracts modulated cadmium mediated depletion of the antioxidant capacities of rats acutely exposed to cadmium and rising lipid peroxidation profile. Conclusions: Regulation of stress and antioxidant response was the underlying mechanism by which the extracts conferred protection against high dose cadmium insult thus suggesting its potential as a viable therapeutic target against its deleterious effects.

Xianling Gubao Capsule Prevents Cadmium-Induced Kidney Injury

Xianling Gubao Capsule (XGC), a kind of capsule preparation of Chinese herbal officially approved for sale by the National Medical Products Administration (NMPA), has the effect of tonifying kidney and strengthening bones. Although the impact of XGC in treating bone diseases has been widely studied, the effect of XGC in kidney injury is unknown yet. The kidney injury model is established by intraperitoneal injection with cadmium chloride (CdCl2). Before model establishment, each XGC group was pregavaged with XGC for 10 d. After 10 d, CdCl2 was injected intraperitoneally into the model group and each XGC group, each XGC group continued to be gavaged with XGC for 4 weeks, and the control group was gavaged with equal doses of distilled water once daily. The level of serum urea nitrogen (BUN) and serum creatinine (Cr) is evaluated by kit. The effect of XGC on protecting kidney injury in mice with kidney injury is analyzed by histopathology (HE stain), immunohistochemistry (IHC), and real-time fluorescence quantitative PCR (RT-qPCR). The results show that CdCl2 significantly increases the level BUN and Cr in serum and results in remarkable pathological changes in the nephron, including tubule edema, congestion, and necrosis. While oral administration of XGC can significantly decrease BUN and Cr in serum and prevent and protect the kidney from the above injuries. In addition, the protein expression of p-mTOR was remarkably reduced, and the ratio of LC3II/LC3I protein and mRNA was significantly increased in mice with oral administration of XGC. Our findings suggest that XGC can prevent and protect kidney injury by improving the state of renal tubular hyperemia and necrosis and reduce the level of BUN and Cr in cadmium poisoning mice.

Influence of water pH in the hepato- and nephrotoxicity of chronic cadmium poisoning in Wistar rats

Introduction: Cadmium is a heavy metal found in the environment that is used industrially; however, it also causes hepato- and nephrotoxic effects. Objective: To evaluate the effect of drinking water pH on the hepato- and nephrotoxicity caused by chronic cadmium poisoning. Material and Methods: We used 90 adult, male Wistar albino rats divided into 6 groups (n = 15): GC5 received a solution of cadmium chloride in drinking water with an acidic pH (pH 5.0); GC7 received a solution of cadmium chloride (400 mg/L) in drinking water with a neutral pH (pH 7.0 water); GC8 received a solution of cadmium chloride in water with an alkaline pH (pH 8.0); GWC5 received drinking water with an acidic pH (pH 5.0); GWC7 received drinking water with a neutral pH (pH 7.0); GWC8 received drinking water with an alkaline pH (pH 8.0). The animals were euthanized 6 months after the start of the experiment. We performed tests for hepatic and renal function and conducted liver and renal histopathology. Results: Water with an acidic pH caused alterations in ALP, ALT and urea in animals exposed to cadmium (P<0.05). In the liver, the majority of animals from the GC7 (57.1%) and GC5 (53.3%) groups showed diffuse microvesicular steatosis, while other groups showed no steatosis (P>0.05). In the kidney, the majority of animals from the GC7 (78.6%) and GWC5 (71.4%) groups showed tubular hydropic degeneration; however, these data were only statistically different from the GWC7 group (P<0.05). Conclusion: Exposure to cadmium in water with an acidic pH led to higher elevations of serum ALP, AST and urea, suggesting that the pH of drinking water influences the hepato- and nephrotoxic effects of this heavy metal.

ASSESSMENT OF THE FUNCTIONAL STATE OF THE LIVER AND KIDNEYS OF LABORATORY ANIMALS AFTER EXPOSURE TO CADMIUM IN A SUB-EXPERIMENT

The paper presents the results of studies of metabolic changes in the blood serum of rats on the background of oral administration of cadmium chloride for 2 months. Elevated serum hepatic enzymes are the main indicator of damage to hepatocytes caused by cadmium poisoning. It was shown that in three experimental groups of rats, which were intragastrically injected with CdCl2, the level of activity of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase was significantly increased compared to the control; on average, the increase in biochemical parameters was 31.8%, 12.9% and 21.9%, respectively. A decrease in the alkaline phosphatase activity in the blood serum of experimental animals, depending on the increase in the dose of the pollutant, is a consequence of the degree of heavy metal damage to the epithelium of the bile ducts. High levels of biochemical parameters of the renal profile, uric acid (UA) and urea, due to impaired glomerular filtration are shown. The noted decrease in the concentration of UA (by 22,3 %) in the 1st experimental group of rats to the level of 87,4±11,6 μmol/L, relative to the negative control (112,5±4,0 μmol/L), indicates a general pathology of the urinary systems induced by heavy metal. The revealed deviations in the indicators of the main biochemical markers of liver and kidney damage serve as a reliable argument characterizing cadmium as a pronounced hepato- and nephrotoxicant.

ANALYSIS OF MT2A AND MT3 GENE EXPRESSION IN RAT'S LIVER AND KIDNEY IN RESPONSE TO CADMIUM CHLORIDE POISONING

The aim of this study was to investigate the expression of metallothionein genes in the liver and kidneys of rats with acute cadmium poisoning.Simulation of poisoning with cadmium chloride was carried out on white outbred female rats, divided into 4 groups depending on the dose of the injected toxicant. RNA samples isolated from rat liver and kidneys were used as research materials.The multiplicity of expression of the MT3 gene in the kidneys increased at the lowest dose of CdCl2 , which was used in this experiment (0.029 mg / kg); with increasing dosage, the expression level decreased, but not lower than the control values. Analysis of the expression of the same gene in the liver showed a tendency towards a decrease in the content of transcripts with increasing dose. The frequency of expression of the MT2A gene at higher doses of CdCl2 increased both in the liver and in the kidneys.In the present work, statistically significant dose-dependent changes in the expression multiplicity of metallothionein genes were detected 24 hours after CdCl2 administration. The revealed differences in the level of transcriptional activity of metallothionein genes require further investigation, since there are probably differences in the level of gene expression at earlier and later periods of toxicant action.

The above literatures all proved that the trace elements in the lipid soluble extracts of ants also played a role in the anti-cadmium poisoning

In order to study the quasi black prickly ant extracts antioxidant mechanism, test the completely random method is adopted to 160 rats, and randomly divided into 8 groups, divided into control group, cadmium poisoning group, cadmium and extracts from petroleum ether to black prickly ant group (divided into high, medium and low dose group), cadmium to higher doses of anhydrous ethanol extracts from black prickly ant group, higher dose of petroleum ether to black prickly ant extract group, only higher doses of anhydrous ethanol extracts from black prickly ant group. The mice were fed for 21 days, and the clinical symptoms of the mice were observed every day. On the 22nd day, the liver, spleen, kidney and sexual organs of the mice were dissected and separated, and the organ coefficients of the mice were calculated. After grinding treatment, the contents of MDA, SOD, CAT and T-AOC in kidney and spleen of mice were determined according to the instructions of the kit. Results showed that the mice of the sex organs of liver, spleen, kidney, organ coefficient were elevated compared with control group (P<0.05), cadmium poisoning group mice kidney, spleen MDA levels were elevated compared with control group (P<0.05), cadmium poisoning group mice kidney, spleen SOD, T–AOC,CAT content decreased (P<0.05), The results indicated that the lipid soluble extract of C. nigra had antioxidant ability, and the low and medium dose of lipid soluble extract of C. nigra had less cadmium toxicity than the high doseThe curative effect in mice was remarkable and the anti-inflammatory function was achieved.