Tropical Weight Loss
Tropical Weight Loss
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The present study demonstrated that L-carnitine improved the oxidative stress, renal histopathological changes and the incidence of the apoptosis induced by MSG. Above all, our current investigation highlights the potential role for the use of L-carnitine to inhibit destructive effects of MSG on the kidney tissue.
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Read More »To the best of our knowledge, this study was the first attempt to investigate the significant protective effect of L-carnitine consumption through anti-oxidant and anti-apoptotic properties on the renal tissue to improve damages induced by Monosodium Glutamate. Oxidative stress induces tissue damage through free radical generation and profound lipid peroxidation, as demonstrated by increasing MDA [31]. Several studies have demonstrated that MSG induces oxidative stress by the production of free radicals which could explain the pathophysiology of many disorders and dysfunctions of the tissues [32]. Different mechanisms including DNA damage, promotion of lipid peroxidation, and protein modification are caused by oxidative stress lead to tissue damages which have been implicated in the pathogenesis of various systemic diseases. One of the organs that is highly vulnerable to damage caused by free radicals is the kidney, probably due to the abundance of long-chain polyunsaturated fatty acids in the renal lipids; also, it is accepted that accumulation of ROS leads to acute and chronic renal failure [33, 34]. It has been reported that monosodium glutamate influences the tissue-specific oxidative stress in different organs, especially the liver and kidney [35]. These effects on the liver and kidney probably because these organs are mainly responsible for detoxification of input compounds in the body. Based on our biochemical tests the amount of serum total protein in MSG treated rats significantly decreased, nonetheless BUN, uric acid, and creatinine increased being in line with several studies revealed MSG induced-liver/kidney injuries [36,37,38]. The reduction of serum total protein in MSG treated group may be due to both liver damages and kidney dysfunction. On the other hand, renal pathological analysis showed the destructive and deformities impact of MSG on proximal and distal convoluted tubules. However, future study should determine liver function test and urinary albumin excretion to confirm the reason of reduced serum total protein in MSG treated group. One of the vital cofactors required for transport of long-chain fatty acids into the mitochondria for production of cellular energy is carnitine (β-hydroxy-γ-N-trimethylaminobutyric acid). Beyond its carrier effects, L-carnitine also helps to eliminate the products of fatty acid metabolism and other toxic compounds from the cells [39]. The data have shown that L-carnitine supplementation significantly scavenge free radicals and protect the cells from oxidative stress [31] by decreasing the serum MDA level and increased activity of catalase, GPX, and SOD enzymes. On the other hand, Siktar et al. [40] and Canbolat et al. [41] suggested that L-carnitine intravenous infusion for 2 months could be effective in attenuating the oxidative stress responses. They reported that L-Ca enhanced the antioxidant status (increase in the serum GPX activity, total anti-oxidant capacity, and GSH/GSSG ratio) and improved the performance of the patients undergoing chronic hemodialysis therapy [39]. Several findings demonstrate that L-carnitine treatment inhibits the MDA production and reverses the depletion of GSH as well as erythrocyte antioxidant enzyme activities in CRF animals [42]. These finding are exactly in line with our results. Additionally, accumulation of free toxic compounds such as long chain fatty acid surrounding the mitochondria induces mitochondrial membrane permeability because of mitochondrial membrane depolarization and membrane canals formation. These changes increase the release of cytochrome C from the mitochondria which activates the apoptotic mechanism in the cells by activating the caspase cascades [43]. The release of cytochrome C from the mitochondria leads to production of a caspase-activating complex of cytochrome c, APAF-1, and procaspase-9, triggers the up-regulation of caspase-9, and subsequently increases the expression of caspase-3, followed by the induction of apoptotic events in the cell [44]. It is demonstrated that overexpression of anti-apoptotic Bcl-2 inhibits the cell death by suppressing cytochrome c, which is released in response to pro-apoptotic stimuli. The level of apoptotic or anti-apoptotic Bcl-2 is a factor that plays a crucial role in determining whether or not the cells will undergo apoptosis [45]. It has been indicated that administration of MSG can induce activation of glutamate receptors which triggers the intracellular Ca2+ signaling pathway. When there is an excess of calcium in the organelles including the endoplasmic reticulum, nucleus, and mitochondria, calcium-dependent enzymes, including proteases and endonucleases, like caspases are activated and provide preliminaries for apoptosis [32]. It has been indicated that prolonged administration of MSG (4 mg/g) significantly induces apoptosis in a time- dependent manner in the rat’s thymocyte cells via disturbing the fine balances between prooxidant-antioxidant system, with excessive production of ROS and resulting oxidative stress status [46]. Another study obtained similar data; the researchers revealed that intraperitonially administered MSG (4 mg/g of body weight) induced oxidative stress mediated apoptosis in the thymus cells of rats [47]. However, L-carnitine supplementation ameliorates the accumulation of long chain fatty acid around the mitochondria which could inhibit the mitochondrial membrane depolarization and permeability and ultimately suppresses the cells apoptosis [48, 49]. Also, L-carnitine can decrease the cell apoptosis through inhibiting the activity of caspases, ameliorating oxidative stress, and enhancing antioxidant defense systems [49, 50]. Mutomba et al. showed that L-carnitine could inhibit the activity of an initiator caspase, caspase 8, as well as the processing of caspase 9, thereby effectively inhibiting cleavage and activation of downstream caspases. The use of a simple non-toxic metabolite like carnitine, as an anti-apoptotic agent, is very attractive compared to synthetic inhibitors with inevitable side effects [51]. Previously, Modanloo et al. reported that L-carnitine could protect the human proximal tubule epithelial HK-2 cells from H2O2-induced cell death. The results of this paper showed that mitochondrial dysfunction associated with cell apoptosis including membrane potential loss, down-regulation of Bcl-2 and up-regulation of Bax, activation of caspase-3, and the release of cytochrome c were abrogated in the presence of L-carnitine [52]. Xie et al. also showed that L-Ca decreased cytochrome c release and caspase-3 and caspase-9 activation in the serum-deprived MC3T3-E1 cells [53]. Moreover, the present study demonstrated that treatment with L-carnitine significantly reduced the gene expression of Caspase-9 and significantly increased the gene expression of Bcl-2. We evaluated the renal cell death by focusing on the RNA expression of apoptosis indicators Bcl-2, Caspase-9, and biomarkers of nephropathy (NGAL, KIM-1). It is recommended that special observations tests, covering deoxynucleotidyl transferase dUTP Nick-End-Labeling ( TUNEL ),and BAX/Bcl-2 immunoblotting required to confirm definitely the occurrence of apoptosis in renal tissue. That is could be a related limitation which is can be considered in future studies. In the present study MSG caused a significant increase in renal expression of KIM-1 and NGAL as well as increased serum concentrations of BUN, uric acid, and creatinine. However, treatment with L-Ca in a dose dependent manner significantly reduced KIM-1 and NGAL gene expression. It has been widely accepted that early detection of renal damages is vital to prevent irreparable injuries. Novel biomarkers such as, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) can be good indicators in the assessment of renal damages [54]. The increased expression of KIM-1 as an extracellular protein was found at very high levels on the apical membrane of proximal tubule cells after ischemic and nephrotoxic injury [55]. NGAL may eventually have prognostic value in predicting not only acute, but also chronic, worsening in renal function in patients already affected by chronic nephropathies [56]. Previously it has been reported that curcumin as an anti-oxidant reduce gene and protein expression of KIM-1 and NGAL and alleviate oxidative toxic stress in the kidney tissue of type 1 diabetes rats [17]. Another study revealed that gentamycin induced nephrotoxicity by over-producing of reactive oxygen species and free radicals and significantly increased serum NGAL, KIM-1 and cystatin-c whereas Irbesartan and other angiotensin II blockers reverse this effect and improve renal function through Modulation of oxidative stress and endogenous antioxidant Capacity [57].
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Read More »The renal cyto-architecture undergoes changes with MSG through increased glomerular hyper-cellularity, inflammatory cells infiltration in the renal cortex, tubular cells edema, and eventually renal tubules degeneration. A proposed molecular mechanism of MSG-induced ROS production is that chronic MSG exposure increases the production of Glutamate which may raise the activity of one of the potential ROS generators like α-ketoglutarate dehydrogenase in the rat kidney. On the other hand, increased intracellular calcium level via glutamate receptors can lead to generation of more free radicals and subsequently a rise in lipid peroxidation. Additionally, cystine uptake inhibition leads to decreased GSH levels that may further promote ROS-mediated renal cell damage [58, 59]. On the other hand, our results indicated that administration of L-carnitine significantly ameliorated the kidney tissue damage and renal function markers such as creatinine, BUN and uric acid. It has been shown that the administration of MSG leads to kidney dysfunction, which is in the same line with our results [60]. Moreover, Vercoutere et al. [61] demonstrated that MSG resulted in several alterations in the cell lines of the kidney convoluted tubules and Bowman’s corpuscles which is associated with variations in the tubular reabsorption threshold, renal blood flow, and glomerular filtration rate. It has been shown that these changes can be attributed to the nephrotoxic effect of MSG which causes functional and cellular damage [60]. MSG increased the oxidative stress that leads to kidney tissue and function damage via several mechanisms including: (1) reduced activities of some antioxidant enzymes as catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione (GSH) and increased MDA level in the kidney, (2) increased activity of α-ketoglutarate dehydrogenase, a potential ROS generator, (3) enhanced free radical generation through increased intracellular calcium level, and (4) decreased GSH levels that may increase ROS-induced renal cell damage [12, 14, 60]. Hence, L-carnitine prevents the MSG-induced renal damage through its potential antioxidant effects. It has also been shown that the antioxidant effects of L-carnitine are associated with scavenging free radicals, preventing reactive oxygen species (ROS) formation through maintaining mitochondria integrity in stress condition along with inhibiting ROS-generating enzymes, such as NAPDH oxidases and improving the synthesis of antioxidant enzymes including SOD, GSH, GST, and CAT [62].
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