Studies on the effect of sodium arsenate on the enzymes of carbohydrate metabolism, brush border membrane, and oxidative stress in the rat kidney

Comparative effect of indomethacin (IndoM) on the enzymes of carbohydrate metabolism, brush border membrane and oxidative stress in the kidney, small intestine and liver of rats

“…IndoM induced marked reductions in the activities of several BBM enzymes, ALP, GGTase, LAP and sucrase (a specific marker of mucosal BBM) in the homogenates of renal cortex and medulla and intestine (Table 3) and in BBM preparations isolated from renal cortex and small intestine (Table 4) showed that IndoM has caused alterations in the architecture of BBM especially to that of renal proximal tubules and mucosal BBM from small intestine as observed earlier with other toxicants [22,26,29,38]. When BBM is damaged by toxic insult including IndoM, these enzymes are usually dissociated from damaged BBM and lost in the lumen along with fragmented microvilli and sometimes are excreted into the urine [[23], [24], [25],[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27],38]. IndoM elicited decrease in the activity of acid phosphatase (ACP), a marker enzyme for lysosomes, indicate that lysosomes along with BBM were also significantly damaged by IndoM exposure.…”

“…Inhibition of prostaglandins synthesis and cellular respiration, DNA damage and increase in oxidative stress are considered to be involved in the pathogenesis of IndoM induced toxicity [6,21,8,5,9]. Reactive oxygen species (ROS) and oxidative stress are considered as the most important mechanism of toxicity caused by various drugs and chemicals [[22], [23], [24][1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28]]. We now hypothesized that IndoM exposure induces oxidative stress that causes damage to various cellular membranes including mitochondria and perturbs antioxidant defense mechanism leading to alterations in cellular metabolic functions of various rat tissues.…”

Toxicodynamics of Lead, Cadmium, Mercury and Arsenic- induced kidney toxicity and treatment strategy: A mini review

“…glycolysis, Krebs cycle), amino acid metabolism, choline metabolism, methionine cycle (transmethylation), purine metabolism and degradation of membrane phospholipids contributes to cell apoptosis in As toxicity [ 104 ]. In this context, attribution of profound damages to brush border membrane (BBM), mitochondria of renal proximal tubule could be, due to, perturbed carbohydrate metabolism, decreased TCA cycle, gluconeogenesis and or HMP-shunt pathway alteration [ 105 ]. Moreover, As also regulates the expression of various phase I and phase II aryl hydrocarbon receptors (AhR)-regulated metabolizing enzymes [phase I enzymes {cytochrome P450 1A1 (CYP1A1),CYP1A2} and phase II enzymes {NAD(P)H: quinone oxidoreductase-1 (NQO1), glutathione-S-transferase A1 (GSTA1)}] [ 106 ] ( Fig.…”

Oxidative stress, free radicals, kidney disease and plant antioxidants

“…Likewise, arsenic is other dangerous metal that has different range of toxicity depending on its oxidation state, longtime exposure and chemical form. It is responsible to suppress antioxidative defense system, damage to mitochondria structure, change energy metabolism and in addition increase lipid peroxidation in renal cells (10). Chronic ethanol consumption is another cause of oxidative nephropathy.…”