Behavioural and biochemical changes after simultaneous and post-treatment of vitamin A and D on cadmium toxicity

Sujatha, Rani; Jayakumar, Arumugam R.; Krishnamoorthy, M. S.; Paul, Vanaja; Jayakumar, R.

doi:10.1016/s1382-6689(99)00013-7

Cited by 16 publications

(13 citation statements)

References 34 publications

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“…In particular nearly all DEGs of ribosome and ribosome biogenesis were down‐regulated, suggesting Cd stress really repressed protein synthesis of cells, which is consistent with the conclusion in previous studies by microarray analysis (Hosiner et al ., ). The down‐regulation of vitamins synthesis related genes is also consistent with the previous report that supplementation with vitamins was found an effective way to counter Cd‐induced stress of cells (Sujatha et al ., ; Matovic et al ., ; Bernhoft, ).…”

Section: Discussionmentioning

confidence: 99%

RNA‐Seq identifies redox balance related gene expression alterations under acute cadmium exposure in yeast

Huang

Pan

et al. 2016

Environ Microbiol Rep

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The nonessential metal cadmium can cause cell toxicity and is associated with a range of human diseases including cardiovascular diseases, neurodegenerative diseases and cancers. In this study, cadmium-induced global gene expression profile of yeast was obtained using RNA Sequencing (RNA-Seq) and further analyzed by means of informatics and experiments. A total of 912 Differentially Expressed Genes (DEGs) (FDR of q < 0.01), including 415 Cd-inducible and 497 Cd-repressed genes were identified. Based on the DEGs, 25 cadmium responsive Clusters of Orthologous Group (COG) and three types of cadmium-induced Gene Ontology (GO) including cellular components, molecular functions and biological processes were analyzed in details. Thereafter, 79 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways under cadmium exposure were assigned. Collectively, 108 redox balance related genes were extracted under cadmium exposure. Meanwhile, cadmium exposure lowered cellular Mitochondrial Membrane Potential (MMP) and increased Reactive Oxygen Species (ROS) levels significantly in the context of mitochondrial dysfunction. Furthermore, cadmium exposure increased cellular GSH levels and decreased GSSG levels and also lowered GSSG/GSH ratio of cells, which supports experimentally our claim that the redox balance is the primary mechanism for cadmium toxicity. The results present in this study may provide new strategies for cadmium detoxification and prevention or therapies of cadmium-associated diseases.

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Section: Discussionmentioning

confidence: 99%

RNA‐Seq identifies redox balance related gene expression alterations under acute cadmium exposure in yeast

Huang

Pan

et al. 2016

Environ Microbiol Rep

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“…And our biochemical results also clearly reveal abnormal metabolic profile in liver after Al treatment. As a matter of fact, the elevation in transaminase is encountered in conditions causing hepatocellular damage, loss of functional integrity of the cell membrane and necrosis such as in chemically induced liver injury and elevation in enzymes (Ninh et al, 2003; Sujatha et al, 1999). Thus, it will be relevant to briefly mention the importance of enzymic changes as manifestations of tissue toxicity.…”

Section: Discussionmentioning

confidence: 99%

The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

et al. 2012

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Aluminium (Al) is used in water purification and is also present in several manufactured foods and medicines. Al is known to induce a broad range of physiological, biochemical and behavioural dysfunctions in laboratory animals and humans. This investigation was carried out to investigate the effects of subchronic exposure to Al (as AlCl3) in rats. Sprague-Dawley rats were randomly separated into two groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with Al (as AlCl3, 5 mg/kg body weight) intraperitonally for 10 weeks. Animals were killed and blood samples were analyzed for blood serum alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) enzyme activities and creatinine, urea (U) and uric acid (UA) levels for evaluating hepatotoxicity and nephrotoxicity. Blood parameters including red blood cells (RBCs), haemoglobin (Hb) concentration, haematocrit (Ht), platelets (PLTs) and white blood cells (WBCs) were compared between control and experimental group to assess haematoxicity. In order to determine the genotoxicity, the number of micronucleated hepatocytes (MNHEPs) was counted in isolated hepatocytes. In addition, histological alterations in liver and kidney samples were investigated. After exposure with Al, the enzymatic activities of ALP, AST, ALT and LDH, and the levels of U and UA significantly increased. RBC, WBC, PLT, Hb and Ht revealed significant decreases in experimental group compared to the control. AlCl3 caused a significant increase in MNHEPs. Furthermore, severe pathological damages were established in both liver and kidney samples. Subchronic exposure to low doses of Al can produce serious dysfunctions in rat blood, liver and kidney, and exposure to this metal can result in greater damages.

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“…It is also reported that treatment with vitamin A ameliorates the adverse effects of cadmium when cadmium is given simultaneously or as a post-treatment (Sujatha et al, 1999). (Sharma et al, 2014).…”

Section: F I G U R Ementioning

confidence: 98%

Caffeine versus antioxidant combination (Antox) and their role in modifying cadmium‐induced testicular injury in adult male albino rats

Labib

Galal

2020

Andrologia

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The unfavourable outcome of cadmium (Cd) on male fertility, sex hormones' production and sperm criteria have been reported in literature (Medina et al., 2017). Testicular tissue is particularly susceptible to cadmium-induced damage. Cd causes degeneration of rats' epididymis, seminal vesicles and spermatozoa (Sajjad et al., 2014). Cd, other heavy metals and oestrogenic-based compounds may explain the recent deterioration in male fertility in industrialised regions in the form of sperm count and testicular function reduction. This may involve the fact that Cd disrupts endocrine control of testicular tissue and induces oxidative damage (Siu et al., 2009). Cd exposure is linked with the generation of free radicals in acute toxicity and reactive oxygen species (ROS) in chronic toxicity. Cdgenerated superoxide anion, hydrogen peroxide and hydroxyl radicals have been reported and are usually associated with redox reactions and ROS-related genetic alterations. It is, therefore, stated that oxidative damage plays an integral part in cadmium toxicity (Liu et al., 2009). In rats subjected to prenatal Cd exposure, plasma testosterone concentrations are drastically lowered and expression of

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Behavioural and biochemical changes after simultaneous and post-treatment of vitamin A and D on cadmium toxicity

Cited by 16 publications

References 34 publications

RNA‐Seq identifies redox balance related gene expression alterations under acute cadmium exposure in yeast

RNA‐Seq identifies redox balance related gene expression alterations under acute cadmium exposure in yeast

The genotoxic, hepatotoxic, nephrotoxic, haematotoxic and histopathological effects in rats after aluminium chronic intoxication

Caffeine versus antioxidant combination (Antox) and their role in modifying cadmium‐induced testicular injury in adult male albino rats

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