Livolin Forte Ameliorates Cadmium-Induced Kidney Injury in Wistar Rats

Abstract

Th e kidney, which is an integral part of the drug excretion system, was reported as one of the targets of cadmium toxicity. Early events of cadmium toxicity in the cell include a decrease in cell membrane fl uidity, breakdown of its integrity, and impairment of its repair mechanisms. Phosphatidylcholine and vitamin E have a marked fl uidizing eff ect on cellular membranes. We hypothesized that Livolin forte® (LIV) could attenuate kidney damage induced by cadmium in rats. Twenty-fi ve adult male Wistar rats were divided into fi ve groups of fi ve rats each: group I (control group) received 0.3 ml/kg/day of propylene glycol for six weeks; group II was given 5 mg/kg/day of cadmium (Cd) i.p for 5 consecutive days; group III rats were treated in a similar way as group II but were allowed a recovery period of 4 weeks; group IV was treated with LIV (5.2 mg/kg/day) for a period of 4 weeks after inducing renal injury with Cd similarly to group II; and group V was allowed a recovery period of 2 weeks after a 4-week LIV treatment (5.2 mg/kg/day) following Cd administration. A significant increase in plasma creatinine, urea, uric acid, and TBARS were observed in groups II and III compared to the control rats. Signifi cant reductions in total protein, glucose, and GSH activity were also recorded. Th e urine concentrations of creatinine, urea, and uric acid in groups II and III were signifi cantly lower than the control group. Th is fi nding was accompanied by a signifi cant decrease in creatinine and urea clearance. Post-treatment with LIV caused signifi cant decreases in plasma creatinine, urea, uric acid, and TBARS. Signifi cant increases in total protein, glucose, and GSH activity of groups IV and V were observed compared to group II. A signifi cant increase in urine concentrations of creatinine, urea, and uric acid and signifi cant decreases in total protein, glucose, and GSH activity were observed in groups IV and V compared to group II. Photomicrographs of the rat kidneys in groups IV and V showed an improvement in the histology of their renal tissue when compared to group II, with features similar to the control rats. Additionally, group III showed an improvement in the histoarchitecture of the kidney compared with group II, although occasional atrophy of some glomeruli and shrinking of renal corpuscles was observed.

Effects of garden egg, carrot and oat-supplements on biochemical parameters in cadmium exposed rats

“…The result of the present study indicates that the administration of Cd induces peroxidative injury in the liver, kidney and intestine of rats, which is mediated by the inhibition of SOD activity and increase in the level of lipid peroxidation (Table 2). This is consistent with findings of previous studies (Asagba et al, 2004;Asagba and Eriyamremu, 2007;Ding et al, 2013, Nazima et al, 2015Ayala et al, 2014;Akomolafe et al, 2016, Oyinloye et al, 2016. One of the mechanisms attributed for the inhibition of SOD by Cd is the displacement of essential metals such as copper and zinc from the enzyme (SOD) and the inhibition of SOD activity might lead to oxidative stress (Timbrell, 1995).…”

Effects of Mining Activities on Gerbillus nanus in Saudi Arabia; A Biochemical and Histological Study

“…In addition, Cd can inhibit complex III of the mitochondrial electron transport chain [48]. The observed nephrotoxicity in this study was associated with glomerular degeneration which has been shown in rats exposed to Cd [49]. Furthermore, the lungs represent one of the main routes through which Cd enters the body [40].…”

Baicalein ameliorates cadmium-induced hepatic and renal oxidative damage in rats

“…In this study we observed that MDA was markedly increased in rats exposed to Cd, thus proposing an increased oxidative stress. Comparable information had already been reported (Akomolafe et al, 2016). Increased MDA level due to Cd exposure could be because of excessive free radicals formatted which do harm to biological macromolecules (Stohs et al, 2001).…”

“…Cadmium decreased nutrient assimilation and retention through its immediate impact on the intestinal mucosal cells. Additionally, exposure to low levels of heavy metals may do harm to the glucocorticoid system (Akomolafe et al, 2016). The glucocorticoid hormones assume an indispensable part in glucose regulation except carbohydrate, lipid, and protein metabolism.…”

“…The increase of GSH could be explained by its incitement to neutralize the increased oxygen free radicals production. On the contrary, Akomolafe et al (2016) watched that Cd prompted GSH level diminished. This may be due to relationship with the given dose and time exposure.…”