Protein Malnourished Rats Research Articles

Ivabradine restores tonic cardiovascular autonomic control and reduces tachycardia, hypertension and left ventricular inflammation in post-weaning protein malnourished rats

Malnutrition results in autonomic imbalance and heart hypertrophy. Overexpression of hyperpolarization-activated cyclic nucleotide-gated channels (HCN) in the left ventricles (LV) is linked to hypertrophied hearts and abnormal myocardium automaticity. Given that ivabradine (IVA) has emerging pleiotropic effects, in addition to the widely known bradycardic response, this study evaluated if IVA treatment could repair the autonomic control and cardiac damages in malnourished rats. Aim: Assess the impact of IVA on tonic cardiovascular autonomic control and its relationship with hemodynamics regulation, LV inflammation, and HCN gene expression in post-weaning protein malnutrition condition. Main methods: After weaning, male rats were divided into control (CG; 22 % protein) and malnourished (MG; 6 % protein) groups. At 35 days, groups were subdivided into CG-PBS, CG-IVA, MG-PBS and MG-IVA (PBS 1 ml/kg or IVA 1 mg/kg) received during 8 days. We performed jugular vein cannulation and electrode implant for drug delivery and ECG registration to assess tonic cardiovascular autonomic control; femoral cannulation for blood pressure (BP) and heart rate (HR) assessment; and LV collection to evaluate ventricular remodeling and HCN gene expression investigation. Key findings: Malnutrition induced BP and HR increases, sympathetic system dominance, and LV remodeling without affecting HCN gene expression. IVA reversed the cardiovascular autonomic imbalance; prevented hypertension and tachycardia; and inhibited the LV inflammatory process and fiber thickening caused by malnutrition. Significance: Our findings suggest that ivabradine protects against malnutrition-mediated cardiovascular damage. Moreover, our results propose these effects were not attributed to HCN expression changes, but rather to IVA pleiotropic effects on autonomic control and inflammation.

L- Carnitine mitigates infertility induced by lithium and carbamazepine in protein malnourished rats

L- Carnitine mitigates infertility induced by lithium and carbamazepine in protein malnourished rats

Comparative study on the possible protective effect of boswellic acids and/or co-enzyme Q10 against stress-induced peptic ulcer in normally fed and protein malnourished rats

Comparative study on the possible protective effect of boswellic acids and/or co-enzyme Q10 against stress-induced peptic ulcer in normally fed and protein malnourished rats

The neural basis of attentional alterations in prenatally protein malnourished rats.

Protein malnutrition during gestation alters brain development and produces specific behavioral and cognitive changes that persist into adulthood and increase the risks of neuropsychiatric disorders. Given evidence for the role of the prefrontal cortex in such diseases, it is significant that studies in humans and animal models have shown that prenatal protein malnutrition specifically affects functions associated with prefrontal cortex. However, the neural basis underlying these changes is unclear. In the current study, prenatally malnourished and control rats performed a sustained attention task with an unpredictable distractor, a task that depends on intact prefrontal cortical function. Radiolabeled 2-deoxyglucose was used to measure neural and brain network activity during the task. Results confirmed that adult prenatally malnourished rats were more distractible than controls and exhibited lower functional activity in prefrontal cortices. Thus, prefrontal activity was a predictor of task performance in controls but not prenatally malnourished animals. Instead, prenatally malnourished animals relied on different brain networks involving limbic structures such as the hippocampus. These results provide evidence that protein reduction during brain development has more wide-reaching effects on brain networks than previously appreciated, resulting in the formation of brain networks that may reflect compensatory responses in prenatally malnourished brains.

Effect of DHA Supplementation on The MDA and SOD Levels in Protein Malnourished Rats

Protein malnutrition interferes with the synthesis of enzymes served as antioxidants while reducing antioxidants concentration in tissues, leading to oxidative stress. One of the most stable markers of oxidative stress is malondialdehyde (MDA). Docosahexaenoic acid (DHA) has an important role in inhibiting oxidative stress and protecting the tissue from peroxidative damage to lipids and proteins, thereby reducing oxidative stress in the tissue. This study aimed to analyze the effect of DHA on the MDA and superoxide dismutase (SOD) levels in protein malnourished rats. This study was carried out using the rat model Rattus norvegicus. After delivery, the rats were classified into two groups, namely, the malnutrition group (MG) and the non-malnutrition group (NMG). The MG was given low-protein diet since birth until 50 days old. The MG was further classified into two subgroups, namely the control malnutrition group with normal feed recovery (CMG), and the treated malnutrition group with normal feed recovery and DHA supplementation for 6 weeks (TMG). At the end of treatment, the blood MDA and SOD levels were assessed. The results showed that the MDA levels in the NMG, CMG, and TMG were 812.75 μM, 647.75 μM, and 624.00 μM respectively. The SOD levels were 19.40 μM, 19.20 μM, and 26.80 μM, respectively. The Kruskal Wallis test showed a significant difference in MDA levels between groups (p = 0.001). The posthoc test using the Mann Whitney test showed that the MDA level in TMG was significantly different from that in NMG, but not significantly different from CMG. The Anova test showed a significant difference in SOD levels between groups (p = 0.000). The Tukey posthoc test showed that the SOD level in TMG was significantly different from that in NMG and CMG. DHA has been shown to play an antioxidant role in malnutrition. DHA can increase the levels of SOD enzymes so that oxidative stress that occurs in malnutrition can be reduced. This is proven by the decrease in MDA levels as a lipid peroxidation product. It can be concluded that DHA supplementation can reduce the MDA levels and increase the SOD levels in protein malnourished rats.

Maternal physical activity prevents the overexpression of hypoxia-inducible factor 1-\u03b1 and cardiorespiratory dysfunction in protein malnourished rats

Maternal physical activity attenuates cardiorespiratory dysfunctions and transcriptional alterations presented by the carotid body (CB) of rats. Rats performed physical activity and were classified as inactive/active. During gestation and lactation, mothers received either normoprotein (NP-17% protein) or low-protein diet (LP-8% protein). In offspring, biochemical serum levels, respiratory parameters, cardiovascular parameters and the mRNA expression of hypoxia-inducible factor 1-alpha (HIF-1α), tyrosine hydroxylase (TH) and purinergic receptors were evaluate. LP-inactive pups presented lower RF from 1st to 14th days old, and higher RF at 30 days than did NP-inactive and NP-active pups. LP-inactive pups presented with reduced serum protein, albumin, cholesterol and triglycerides levels and an increased fasting glucose level compared to those of NP-inactive and NP-active groups. LP and LP-inactive animals showed an increase in the cardiac variability at the Low-Frequency bands, suggesting a major influence of sympathetic nervous activity. In mRNA analyses, LP-inactive animals showed increased HIF-1α expression and similar expression of TH and purinergic receptors in the CB compared to those of NP groups. All these changes observed in LP-inactive pups were reversed in the pups of active mothers (LP-active). Maternal physical activity is able to attenuate the metabolic, cardiorespiratory and HIF-1α transcription changes induced by protein malnutrition.

Prenatal Protein Malnutrition Produces Resistance to Distraction Similar to Noradrenergic Deafferentation of the Prelimbic Cortex in a Sustained Attention Task.

Exposure to malnutrition early in development increases likelihood of neuropsychiatric disorders, affective processing disorders, and attentional problems later in life. Many of these impairments are hypothesized to arise from impaired development of the prefrontal cortex. The current experiments examine the impact of prenatal malnutrition on the noradrenergic and cholinergic axons in the prefrontal cortex to determine if these changes contribute to the attentional deficits seen in prenatal protein malnourished rats (6% casein vs. 25% casein). Because prenatally malnourished animals had significant decreases in noradrenergic fibers in the prelimbic cortex with spared innervation in the anterior cingulate cortex and showed no changes in acetylcholine innervation of the prefrontal cortex, we compared deficits produced by malnutrition to those produced in adult rats by noradrenergic lesions of the prelimbic cortex. All animals were able to perform the baseline sustained attention task accurately. However, with the addition of visual distractors to the sustained attention task, animals that were prenatally malnourished and those that were noradrenergically lesioned showed cognitive rigidity, i.e., were less distractible than control animals. All groups showed similar changes in behavior when exposed to withholding reinforcement, suggesting specific attentional impairments rather than global difficulties in understanding response rules, bottom-up perceptual problems, or cognitive impairments secondary to dysfunction in sensitivity to reinforcement contingencies. These data suggest that prenatal protein malnutrition leads to deficits in noradrenergic innervation of the prelimbic cortex associated with cognitive rigidity.

Vitamin B6 improves blood parameters in rats fed a protein-deficient diet and subjected to moderate, long-term exercise.

Vitamin B6 is necessary for many enzymatic pathways (glucose and lipid metabolism, DNA/RNA synthesis, or modulation of gene expression) and affects immune cell function and blood-forming processes. We hypothesised that supplementing a protein-deficient diet with vitamin B6 may reduce the negative impact of protein malnutrition. Here, we evaluated the effect of moderate, long-term exercise (ninety days) on selected blood parameters in rats fed a normal diet, a protein-deficient diet, or a protein-deficient diet supplemented with vitamin B6. Selected haematological, immunological, and biochemical parameters were examined. A protein-deficient diet lasting 90 days caused significant reduction in body mass, increased activity of aminotransferases (asparagine and alanine), an increased percentage of innate cells in the blood, and decreased haemoglobin concentration in the blood. Adding vitamin B6 significantly increased body and muscle mass, decreased liver parameters, and caused normalisation of haemoglobin concentration and the proportion of white blood cells in the blood. These results indicate that vitamin B6 supplementation significantly improves the health of protein-malnourished rats and paves the way for the development of novel anti-malnutrition therapies.

Effects of Parenteral Amino Acid Administration on the Postoperative Nutritional Status and Wound Healing of Protein-Malnourished Rats

In Japan, parenteral nutrition (PN) solutions are frequently administered to patients in the postoperative short-term period. In these cases, amino acid-containing peripheral parenteral nutrition (PPN) solutions, amino acid-free maintenance solutions or combinations of the two are used. However, consensus regarding the most beneficial solution for these patients is lacking. Here, we examined the nutritional status and wound healing outcomes in protein-malnourished rats receiving postoperative administrations of PPN solution, maintenance solution or combinations of the two solutions. Protein malnutrition was induced in Sprague-Dawley rats by feeding an AIN-93G-based low-protein diet (5% casein) for 2 wk. After laparotomy, dorsal skin incision, and placement of a jugular vein catheter, the rats were divided into 3 groups. Each group was administered 113 kcal/kg/d, with group A receiving maintenance solutions without amino acid, group B receiving PPN with 1.5% amino acid, and group C receiving PPN with 3% amino acid. After 5 d post-operative administration, we measured the tensile strength of the wound area, skeletal muscle weights, and nutritional parameters. Significantly higher plasma nutritional parameters and gastrocnemius and extensor digitorum longus (EDL) muscle weights were observed in groups B and C than in group A. Group C exhibited significantly elevated tensile strength of the wound area along with up-regulation of type I collagen mRNA expression compared to group A. These findings demonstrate the nutritional status and wound healing benefits of short-term postoperative administration of PPN solutions containing amino acids in protein-malnourished rats.

Effects of Cadmium Toxicity on Bio-distribution of Trace Elements in Normal and Protein Malnourished Rats

Effects of Cadmium Toxicity on Bio-distribution of Trace Elements in Normal and Protein Malnourished Rats

Influence of L-arginine on Cisplatin-Induced Hepatotoxicity in both normally Fed and Protein Malnourished Rats

Liver has great capacity to detoxify toxic substances and synthesized useful principles. Therefore, damage to the liver inflicted by hepatotoxic agents is of grave consequences. Protein malnutrition produces profound effects on biochemistry and physiology of the body as well as growth failure of most body organs. Cisplatin is a member of anticancer drugs that elicits many hepatotoxicity. The study was carried out to investigate the possible hepato-curative and hepato-protective effect of l-arginine either alone or in combination with silymarin against hepatotoxicity resulted from cisplatin (7.5 mg/kg i.p.) treatment in normally fed and protein malnourished male albino rats. All treatments were administered for 5 consecutive days (l-arginine, 200 mg/kg i.p.) and (silymarin, 100 mg/kg i.p.) after and before cisplatin injection. In the cisplatin group, the results revealed significant decrease in the body weight and increase in alanine aminotransferase and aspartate aminotransferase, as well as liver body weight ratio. Antioxidant status was suppressed as manifested by significant decline in reduced glutathione content and total protein level along with decreased enzymatic activity of super oxide dismutase and increased lipid peroxidation, nitric oxide, an effect that was enhanced by combination with protein malnutrition. Administration of l-arginine was effective in decreasing cisplatin hepatotoxicity that restore of anti-oxidant machinery and blunting of mounted malondialdehyde levels. Moreover, histological examination demonstrated that l-arginine significantly reduced cellular infiltration, congestion blood vessels, degenerative changes in hepatocytes and fatty changes. It is concluded that the combined administration of l-arginine with silymarin represents a promising strategy to restrain the cisplatin hepatotoxicity.

Comparative Study on the Influence of Epigallocatechin-3-gallat e and/ or Coenzyme Q10 against Alzheimer's disease Induced by Aluminium in Normally-Fed and Protein Malnourished Rats

Background: Alzheimer’s disease (AD) is a neurodegenerative disorder greatly influenced by oxidative stress and mitochondrial dysfunction which may lead to deposition of β-amyloid (Aβ) peptides. Protein malnutrition increases oxidative damage in cortex, hippocampus and cerebellum. Epigallocatechin-3-gallate (EGCG) has health-promoting effects in CNS, while Coenzyme Q10 (CoQ10) is intracellular antioxidant and mitochondrial membrane stabilizer. Objective: To investigate the possible protective effect of EGCG and/or CoQ10 against aluminium-induced neurotoxicity presenting symptoms that mimic AD in both normally-fed (NF) and protein malnourished (PM) rats. Methods: Ten groups of rats were used; five for NF (20% casein) and the same for PM (10% casein). Both NF and PM groups received daily for four weeks; either saline for control or AlCl3 (70 mg/kg, I.P) for AD induction groups, treated groups received together with AlCl3 either EGCG (10 mg/kg, I.P), CoQ10 (200 mg/kg, P.O) or combination of both. Histopathological changes in the brain and biochemical changes in Aβ, Acetyl cholinesterase (ACHE) as well as oxidative parameters (MDA, SOD, TAC) were evaluated for all groups. Results: The study revealed that, brain neurological damage characterizing induction of AD as indicated by histopathological changes in the brain and the increase in Aβ, ACHE and MDA as well as the decrease in SOD and TAC was more pronounced in PM rats. Administration of EGCG and/or CoQ10 during induction of AD showed protective effect in both NF and PM rats as indicated by the decreased Aβ, ACHE, MDA together with the increased SOD, TAC and confirmed by histo pathological examinations in different brain regions. However, the effect of combined treatment was more pronounced in both NF and PM rats. Conclusion: PM is a risk factor in induction of AD, EGCG and CoQ10 combined therapy has marked protective effects during induction of AD in both NF and PM rats rather than each individual treatment.

Protective Effect of Zinc against Postnatal Lead-Induced Alterations in the Neurobehavioral Development of Normally-Fed and Protein Malnourished Rats

Background: The most critical effects of lead (Pb) toxicity occur among children exposed during fetal development, postnatal development or both. Malnutrition is a common problem worldwide and occurs in both developing and developed countries. Zinc is an essential mineral and a fundamental component of the endogenous enzymatic antioxidant system. Objective: To evaluate the possible protective effects of zinc against postnatal Pb-induced alterations in the physical and neurobehavioral development in both normally-fed (NF) and protein malnourished (PM) rats. Methods: Protein sufficient diet (20% casein) for NF groups and protein deficient one (8% casein) for PM groups were utilized. Both NF and PM groups were subdivided to 3 groups 6 dams/each and received daily from parturition until weaning (together with diet); saline for control, 1 ml lead acetate (12 mg/ml) and zinc sulphate (32 mg/kg) with Pb. Pups were evaluated for physical and neurobehavioral development as well as for performance in Neonatal T-maze and Open-field test (OFT). Results: Postnatal Pb exposure inhibited most physical and neurobehavioral development of both NF and PM pups. It also reduced number of correct choices as well as ambulation and rearing frequencies in both pups, the effect was more pronounced in PM pups. However, Zinc increased these parameters in NF and PM pups but increased body weight, ambulation and rearing frequencies while decreased time of appearance of eye opening and grooming time in NF pups only. Conclusion: Postnatal Pb exposure caused alteration in some aspect of physical and neurobehavioral development as well as in some behavioral functions as learning, emotionality as well as locomotor and exploratory activities. The alterations were much greater under the condition of protein malnutrition. Zinc was shown to protect against these lead-induced alterations in both NF and PM rat pups. However the protective effect of Zinc sometimes declined under concomitant protein malnutrition.

Curcumin protects against nicotine-induced stress during protein malnutrition in female rat through immunomodulation with cellular amelioration.

Nicotine aggravates many chronic inflammatory disorders in females under the protein-malnourished conditions because women are more susceptible to nicotine-induced diseases due to their low innate immunity. Although curcumin have been found to obliterate the nicotine-induced disorders through its anti-nicotinic activity under the protein-malnourished condition, the exact mechanism of protective action of curcumin is still unclear. Female Wister rats maintained under the normal and protein-restricted diets in two separate groups were injected with the effective dose of nicotine-tartrate (2.5mg/kg body weight/day, subcutaneously) and supplemented with the effective dose of curcumin (80mg/kg body weight/day, orally) for 21days. The morphology of red blood cells (RBCs), molecular docking, lipid profile and activities of antioxidant enzymes in tissues, cytokines profiling (T helper cell type 1; and T helper cell type 2), mRNA and protein expression of cytokines, transcription factors (activator protein 1), regulatory molecule (P(53)), growth factors (Granulocyte-macrophage colony-stimulating factor; Transforming growth factor beta) were determined to establish the mechanism of actions of curcumin against the nicotine-mediated stress in the protein-malnourished rats. This study revealed that curcumin bound to the Histidine 87 residues of haemoglobin with a greater binding affinity and significantly protected the RBCs against nicotine-induced damage. Furthermore, the nicotine-mediated disruption of Th1/Th2 balance through upregulation and downregulation of different factors was effectively restored by curcumin under the protein-malnourished conditions. The study demonstrated that curcumin was a potent protective compound against the nicotine-induced stress and offered a probable biochemical and immunomodulatory mechanism of protective action of curcumin.

Hemotoxic effects of cadmium in normal and protein malnourished rats

Cadmium is chemically related to zinc and found wherever zinc occurs in nature. Cadmium is emitted to air and water by mines, metal foundries, viz. brass and industries using Cadmium in alkaline accumulators, alloys, paints and plastics. Cadmium exposure results in increase of concentration of a protein, called metallothionein, which plays an important role in detoxification of heavy metals. In persons not exposed to high amounts of cadmium, the concentration of cadmium in blood, bound mainly to red blood cells, is very small, less than 1 µg/100 mL whole blood. Gontzea and Popescu1 revealed that rats reared on low protein (casein 8.8%) diet were more susceptible to the adverse effects (blood and liver enzyme parameters) of injected Cd, than control given a diet with 17.8% casein. The present study was conducted on rats maintained on normal (21% protein) and protein malnourished (8% protein) diets. Exposure to cadmium in growing rats induced structural anomalies in the erythrocytes and leukocytes. Microcytic hypochromic anemia with erythrocytopenia and leukocytopenia were evident. Protein malnutrition appears to enhance the vulnerability of the animals to these changes.

Simvastatin increases liver branched-chain α-ketoacid dehydrogenase activity in rats fed with low protein diet.

The rate-limiting step in branched-chain amino acids (BCAAs) disposal is catalyzed by the mitochondrial branched-chain α-ketoacid dehydrogenase complex (BCKDH). BCKDH activity is regulated mainly by a reversible dephosphorylation (activation)/phosphorylation (inactivation) cycle catalyzed by a specific phosphatase (BDP) and kinase (BDK). Current catalytic activity of BCKDH, described as BCKDH activity state, and thus also BCAAs catabolic rate depend directly on the portion of BCKDH occurring in its active dephosphorylated form. Liver BCKDH activity state alters in response to different nutritional factors. Feeding rats a low-protein diet decreases BCKDH activity. It has been previously shown that lipid lowering drugs, fibrates upregulate liver BCKDH activity and stimulate BCAAs catabolism, especially under the condition of dietary protein deprivation. Effect of statins on liver BCKDH activity has not been studied yet. The present study was aimed at investigating the in vivo effect of simvastatin on liver BCKDH activity, as well as E1, E2 and BDP and BDK mRNA levels in rats fed with either a standard (23% protein) or a low protein (8% protein) diet. For 14 days, simvastatin (80 mg/kg b wt/day) or the vehicle (0.3% methylcellulose) were administrated orally by gavage to the treated and control groups, respectively. The actual BCKDH and total BCKDH activities were assayed spectrophotometrically prior to and following incubation with lambda phosphatase, respectively. The mRNA levels of the selected genes were quantified by means of a semi-quantitative RT-PCR. In rats fed with the low protein diet simvastatin administration reversed physiological adaptation of liver BCKDH to protein restriction and increased liver BCKDH activity state by 39% (p<0.05). Changes in BCKDH activity did not correspond to any changes in mRNA levels for BCKDH catalytic and regulatory enzymes. On the contrary, in rats fed with standard diet liver BCKDH activity state did not alter substantially in response to simvastatin administration. In conclusion, the obtained results indicate that simvastatin stimulates liver BCKDH activity and BCAAs degradation in rats fed with the low protein diet, whereas it exerts no effect on BCKDH in rats fed with the standard diet. Stimulation of liver BCKDH activity can be attributed to altered phosphorylation status of the complex (increased dephosphorylation), and it is not associated with changes in mRNA levels for complex enzymes. It is conceivable that in protein malnourished rats simvastatin effect on liver BCKDH activity and BCAAs metabolism can contribute to the myotoxicity observed during treatment with this agent.

Probiotics protect the intestinal wall of morphological changes caused by malnutrition.

This study sought to morphometrically analyze the jejunal wall of protein-malnourished rats administered a probiotic supplement. The sample consisted of recently weaned Wistar rats (Rattus norvegicus) distributed among four groups: animals given a commercial diet (G1, n = 4); animals given the same ration as G1 plus a probiotic supplement (G2, n = 4); animals given a 4% protein diet (G3, n = 4); and animals given the same ration as G3 plus a probiotic supplement (G4, n = 4). After 12 weeks, part of the jejunum was harvested and subjected to routine histological processing. Transverse sections with a thickness of 3 µm were stained with HE, and histochemical techniques were used to assay for glycoconjugates, including staining with periodic acid-Schiff (PAS) + diastase, Alcian Blue (AB) solution at pH 2.5, and Alcian Blue solution at pH 1.0. Morphometric analysis of the bowel wall showed that the probiotic culture used in this study induced hypertrophy of several layers of the jejunal wall in well-nourished animals and reduced the bowel wall atrophy usually observed in protein-malnourished animals. Neither malnutrition nor the use of probiotics altered the relationship between the number of goblet cells and the number of enterocytes.

Behavioral Toxicity of Cadmium in Normal and Protein Malnourished Rats (Two-Generation Study)

Assessments of behavioral toxicity of cadmium (Cd, 50 ppm, through drinking water for 120 days) were carried out in growing male rats, maintained on diets containing 21% and 8% protein. The effects of chronic exposure to cadmium toxicity were studied both in Fo and F1 generations. The low protein diet (8%) caused a significant reduction in the litter size, a delay in the physical developmental landmarks like less body weight and eye opening, and also caused marked delay in the development of sensory–motor reflexes like visual placing, cliff aversion, in the F1 offspring. The viability and lactation indices were not significantly affected. Cadmium exposure resulted in significant growth retardation in both the dietary groups of the Fo–generation rats during the growing, gestation and lactation periods. A significant delay in the development of the criterion response in the ascending wire mesh test was observed in the pups of cadmium exposed malnourished dams only whereas the development of beam balancing ability was significantly delayed in the pups of cadmium exposed dams of both the diet groups but the effect was more marked in the protein malnourished groups. The data indicate the enhanced vulnerability of protein malnourished animals to the behavioral aberrations caused by Cd toxicity.

Physiological slowing and upregulation of inhibition in cortex are correlated with behavioral deficits in protein malnourished rats.

Protein malnutrition during early development has been correlated with cognitive and learning disabilities in children, but the neuronal deficits caused by long-term protein deficiency are not well understood. We exposed rats from gestation up to adulthood to a protein-deficient (PD) diet, to emulate chronic protein malnutrition in humans. The offspring exhibited significantly impaired performance on the ‘Gap-crossing’ (GC) task after reaching maturity, a behavior that has been shown to depend on normal functioning of the somatosensory cortex. The physiological state of the somatosensory cortex was examined to determine neuronal correlates of the deficits in behavior. Extracellular multi-unit recording from layer 4 (L4) neurons that receive direct thalamocortical inputs and layers 2/3 (L2/3) neurons that are dominated by intracortical connections in the whisker-barrel cortex of PD rats exhibited significantly low spontaneous activity and depressed responses to whisker stimulation. L4 neurons were more severely affected than L2/3 neurons. The response onset was significantly delayed in L4 cells. The peak response latency of L4 and L2/3 neurons was delayed significantly. In L2/3 and L4 of the barrel cortex there was a substantial increase in GAD65 (112% over controls) and much smaller increase in NMDAR1 (12-20%), suggesting enhanced inhibition in the PD cortex. These results show that chronic protein deficiency negatively affects both thalamo-cortical and cortico-cortical transmission during somatosensory information processing. The findings support the interpretation that sustained protein deficiency interferes with features of cortical sensory processing that are likely to underlie the cognitive impairments reported in humans who have suffered from prolonged protein deficiency.

Studies on Hepato and Renal Toxicity of Cadmium on Normal and Protein Malnourished Rats

Cadmium is an established toxic metal with its ability to accumulate in blood, liver and kidney. It adversely affects the renal cortex and ultimately leads to the renal failure. It has been reported that deficiency of certain dietary components affects cadmium toxicity. Present study was designed to evaluate the cadmium toxicity (50 ppm in drinking water) in protein malnourished group (8%) and on normal protein (21%) diet groups. It was found that Cd exposure led to marked elevation in alkaline phosphatase, acid phosphatase, glutamic pyruvic transferase, glutamic oxaloacetic acid transferase with significant increase in protein malnourished group (p 0.005). Same trend of result was noted in urinary concentration of alpha amino acid, albumin, total protein and glucose. Results were more significant (p 0.001) in malnourished animals. However, hepatic and renal enzymes showed depletion in all groups. There was marked increase in serum enzymes GOT, GPT, alkaline phosphatase, acid phosphatase in low protein diet + Cd (p 0.001). Hence present findings strongly support that protein under-nutrition predisposes the organism to the deleterious effects of cadmium toxicity.