Depletion Of Cd-Group Case Study

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

TCDD is a dioxin that can be produced through diesel exhaust, burning waste, and chemical manufacturing. In recent years, many have argued that exposure to this chemical can cause serious illnesses. Studies on animals have shown that TCDD is one of the most poisonous chemicals out there. The animal testing has been found to be especially toxic to developing babies in the womb. A pregnant rat given a dose of less than one part per billion (which is comparable to a single drop in 14,000 gallons of water) will cause female sexual characteristics in a male embryo. Doses of 100 parts per billion in rodents and fish have been proven to cause birth defects such as cleft palates, malfunctioning kidneys, heart problems, and weak bones (Schmidt). Animal studies have proven that small doses of TCDD can be severely detrimental to one’s

These substances not only trigger liver, heart, kidney and nervous system deterioration, but also cause lung impairment and cancer.

findings that exposure to DDE, the chemical compound that’s left when DDT breaks down, is linked to AD (4).

The high-dose I+ exposure significantly induced the expression of sphingosine-1-phosphate phosphatase 1 (SGPP1), a gene encodes a key enzyme that catalyzes the degradation of S1P to long-chain ceramides [21], at three time points (6h: FC=1.62; 12h FC=1.58 and 24h: FC=2.00, p-value and FDR< 0.01 at three time points). Without the cytokine mix, the high-dose I the elevated expression of SGPP1 started after 12h of incubation (12h FC=1.42 and 24h: FC=1.5, p-value and FDR< 0.01 at both time points). After exposure to the high-dose I+, the expression of the ceramide synthase 6 (CERS6), encoding the enzyme that catalyzes the synthesis of ceramide [40], was first decreased at 12 h (FC=-1.28, p-value=0.02 and FDR=0.054) and followed by a considerable

Due the fact of the highly toxic chemical, Dioxin can cause cancer, reproductive and developmental problems, damage to the immune system, possibly disturbances

2,3,7,8-TCDD is one of the most toxic chlorinated dibenzo-p-dioxins, CDDs, known to affect mammals, according to the Agency for Toxic Substances and Disease Registry’s report in 1998 (ATSDR, 1998, p. 2). TCDD can be formed during certain manufacturing processes. It is most commonly created during the chlorine bleaching process or during the creation of chlorinated phenols. Then, the 2,4,5- trichlorophenol which is created from TCDD can be further reacted in order to produce hexachlorophene or 2,4,5-trichlorophenoxyacetic acid, chemicals which are respectively a bactericide and an herbicide.

Urate functions as a pro-oxidant and antioxidant in human serum, the mechanisms for the pro-oxidant effects of urate are poorly understood. In humans urate builds up in our serum as a result of dietary purine. Urate is an antioxidant of reactive oxygen species, yet, high serum urate (hyperuricemia) is associated with inflammatory diseases. There is a strong association for urate with gout, metabolic syndrome and cardiovascular disease. The link between hyperuricemia and inflammatory disease is oxidative stress. Urate acts as a pro-oxidant by increasing reactive oxygen species and enabling the oxidation of LDL. Urate’s switch from antioxidant to pro-oxidant might be triggered by high serum urate, ergo the ‘dose makes the poison’.

Mixed contamination of benzo[a]pyrene (B[a]P), arsenic (As), cadmium (Cd), and lead (Pb) is a major environmental and human health concern. The mixture toxicity data on these co-contaminants are important for their risk assessment. In this study, we have determined the mixture toxicity of As, Cd and Pb and B[a]P with As, Cd or Pb in HepG2 cells. The binary mixtures of Cd + As, Cd + Pb and As + Pb and B[a]P + metals (B[a]P + As, B[a]P + Cd and B[a]P + Pb) were evaluated for their interaction on the cytotoxicity using the MTS assay. A full factorial design (4 × 5) was used to determine the interaction toxicity and all the six mixtures showed significant interaction on the cytotoxicity. We further investigated the role of oxidative stress (reactive

In today’s era the industrialisation, agriculture, domestic activities led to a large amount of wastewater having toxic elements such as lead, mercury, cadmium, copper, arsenic, chromium etc. and carcinogenic organic compounds which has adversely effected human lives, animal lives and environment [1, 2]. In trace amounts, Cr (III) is an essential nutrient for humans and to mammals for their maintenance of normal glucose tolerance factor, lipid and protein metabolism [3]. On the other hand Cr (VI) is very toxic to human as well as marine life and poses various health problems such as liver damage and pulmonary congestion and regarded as carcinogenic also [4-6]. Dinitrophenolic compounds, a group of persistent organic compounds, has received a widespread attention due to its detrimental effects to the environmental and human health [7]. 2,4-Dinitrophenol has been extensively detected in the industrial effluents due to its diverse use as a raw material for speciality chemicals or as an intermediate in textile, dye and pharmaceutical industries [8] which can restrict the cell growth even at low concentration (1 mg L-1).

Animals: Nine Sprague-Dawley male rats aged 50 days, and weighing 605 ± 7.2 g were purchased from Samtako Bio Co. (Osan, Korea). Upon arrival, rats were fed a basal purified diet (standard rodent chow) and housed in individual cages on pine shavings under controlled conditions of light (12h light/12h dark), temperature (22 ± 2 °C) and humidity (50 ± 20%). All experimental procedures were performed according to the national institute guidelines for animal care and use approved by the animal ethics committee of Chungnam National University (approval letter no. CNU-00659). After a week acclimation period, rats (9) were divided into three diet groups based on the EVA concentration for 11 weeks. The control diet (n = 3) comprised standard rodent chow (SeoulFeed Co. Ltd, Incheon, Korea) ground into powder using a laboratory mill. Diet 2 (low-dose, n = 3) was made mixing 3 mg EVA powder/kg b.w with standard rodent chow, and the third diet (high-dose, n = 3) was made mixing 15 mg EVA powder/kg b.w with standard rodent chow. Rats had free access to drinking water during the entire experimental period.

The mechanism by which adenine induces CKD is not well elucidated. Adenine and its metabolite, DHA, have low solubility and precipitate in the renal tubules leading to their occlusion and the development of uremia [7, 14]. It has been reported that, adenine has an affinity to cause several oxidative and inflammatory reactions in renal tissues which might cause an increase in several oxidative and inflammatory markers such as catalase, GSH, SOD [12, 17, 22-24]. Adenin treatment caused oxidative stress within the cells. Which demonstrated by the increase in the oxidative derivative of deoxyguanosine, 8-OHdG, one of the major DNA oxidative products

markers. The aim of this study is to investigate, for the first time, whether the antioxidant properties of

The GSTs family of enzymes (i.e. GSTP1, GSTZ1, GSTM1, and GSTT1) is involved in arsenic metabolism and plays a role in the cellular response mechanism against oxidative stress. Arsenate is reduced to arsenite by two enzymes from the glutathione-S-transferase (GST) family: GSTO1 (Zakharyan et al., 2001) and GSTO2 (Whitbread et al., 2003) that use glutathione (GSH) as a reducing agent (Buchet and Lauwerys 1987) (Figure 1.2.). Arsenite is actively transported inside the cell by aquaporin’s (AQP) cell membrane proteins (Liu et al., 2002) and is then modified by methyltransferases (Marafante and Vahter, 1984) using S-adenosyl-methionine (SAM) as a methyl donor (Buchet and Lauwerys, 1985) to produce monomethylarsonous acid (MMA (III)) and dimethylarsinous acid (DMA (III)). Both become further oxidized to monomethylarsonic acid (MMA (V)) and dimethylarsinic acid (DMA (V)): predominant metabolites in urine (Aphosian and Aphosian, 2006).There are different biomarkers for assessing the genotoxicity. Biomarkers of effects are the quantifiable changes that an individual endures, which indicates an exposure to a compound and may indicate a resulting health effect. Genotoxicity endpoints are followed directly in exposed humans. The most frequently used endpoints includes chromosome aberrations, micronuclei, sister

Oxidative stress is associated with postprandial hyperglycaemia via destroying the natural antioxidant defense of systems and organs 7. SOD activity indirectly reflects the antioxidant capacity, and the level of MDA indirectly reflects the degree of cells damage by oxygen free radical 36. Largely diminished SOD activity and increased MDA content were measured in BGF model compared with other diabetes model according to a previous study 37. Oxidative stress is produced in the skin of diabetic mice with BGF, which accelerates the skin damage 37. Consistently, the level of SOD was lowest while MDA level was highest in the FHG model rats, which might suggest the most severe oxidative stress injury caused by BGF. Furthermore, NO plays important roles in many processes, including immune, cardiovascular and nervous systems 38, 39. Recent evidence suggests that NO can cause net hemodynamic changes through interacting with other vasodilation mediators, such as adenosine and prostacyclin 40.