Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats fed an 18% casein (Cs) or a protein deprived diet (PD) for 8 weeks received injections of Escherichia coli lipopolysaccharides (LPS) in both hind foot pads. While these injections were tolerated in Cs rats, about 50% of PD rats died after 1 or 2 days as a result of a massive necrosis of the liver. To a large extent these lesions were prevented by cortisone. Three days after injection of LPS, Cs rats exhibited a hypertrophy of the popliteal lymph nodes (PLN) and spleen, as well as a drastic increase in DNA synthesis in DNA synthesis in the PLN. Mitotic indices did not increase. The DNA synthetic responses to PLN in the surviving PD rats were much lower than in Cs animals, but a sharp rise in DNA synthesis and mitotic activity occurred in the spleen. The comparison with the effects of LPS in cortisone-treated rats showed that both cortisone-sensitive and -resistant cells participated in PLN activation in rats fed both diets, but that only cortisone-resistant lymphocytes entered mitosis in the spleens of PD rats. LPS also provoked a sharp drop in both DNA synthesis and mitosis in the thymus, probably due to a stress effect, since only cortisone-sensitive thymocytes were involved. In a second experimental series, immunological tests (Rosette-forming cells, Plaque-forming cells, serum hemagglutinin titers) were performed 7 days after intraperitoneal injection of LPS. The responses were not significantly different in Cs and PD rats. This is in contrast with the protein deficiency-induced depression of thymus-dependent humoral immunity.
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PMID:Effects of a protein deprived diet on the hepatotoxicity, and the DNA synthetic, mitogenic, and immunological actions of microbial lipopolysaccharides in the rat. 68 57

Young male rats (100-130 g) were fed diets of equal energy content containing o.5, 1,2,3,5, and 18% lactalbumin consumed either freely or in restricted amounts. The rats receiving low protein diets failed to grow and mature. Those consuming the 0.5 and1% protein diets given freely developed the characteristic features of kwashiorkor including edema, while those receiving the diets in restricted amounts developed the characteristic features of marasmus. The rats fed low protein diets had low plasma levels of essential amino acids; however, the lysine level was well maintained. The plasma levels of nonessential amino acids, especially glycine, alanine, and aspartic and glutamic acids were raised in marasmic rats but were reduced in rats fed low protein diets ad libitum. Young and severly malnourished rats appeared to have limited ability to synthesize urea. Therefore, they excreted more ammonia and other nitrogenous substances such as ethanolamine, and when given an amino acid load, intermediary metabolites of the ingested amino acids. Rats fed low protein diets showed diminution of total liver DNA, RNA, and protein. In addition to the reduction of protein synthesis resulting from decreased cellular RNA, ribosomes from the livers of protein-deficient rats had reduced ability to synthesize proteins. This defect was associated with the detatchment of the ribosomes from endoplasmic reticulum membrane and the elevation of the proportion of monosomes to polyribosomes. Malnutrition did not produce any change in the turnover rate of liver RNA. Protein deficiency caused significant depression of serum insulin, thyroxine, and corticosterone levels. Theoverall conclusion is that mammalian metabolism is well adapted to dietary intake and that this adaptation is achieved through dietary control of synthesis and release of key metabolic hormones.
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PMID:Experimental protein and energy in the rat. 80 70

Dietary protein deficiency is known to modify the response to the pharmacotoxicological activities of drugs and foreign compounds, due in part to altered rates of metabolism. Prediction of whether in vivo susceptibilities to foreign compounds are increased or decreased in protein deficient animals has been said to be related to the relative toxicites of the metabolic products. We have shown that weanling rats fed semipurified casein diets for 15 days show a 75% depression of hepatic microsomal mixed function oxidase activities. About one-fourth of this decrease is due to a retardation of the normal rate of liver cell proliferation and less microsomal protein; the remaining three-fourths is due to a reduction of the specific enzyme activity. This latter decrease is closely correlated with similar decreases in cytochrome P-450 and cytochrome c reductase activities and cytochrome P-450 contents. Although protein deficiency affects the relative contents of phosphatidylcholine and cytochrome P-450, this does not result in modifications of the Km for metabolism, as is seen with phenobarbital administration in the various dietary groups. The depression of mixed function oxidase enzyme activities caused by feeding the protein deficient diet for 15 days can be restored to normal by feeding the 20% casein diets for an additional 30 days in the case of aniline hydroxylase but only partially in the case of ethylmorphine N-demethylase. The complexities of determining the role of metabolism as a modulator of protein deficiency effects on foreign compound toxicity are discussed.
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PMID:The effect of quantity and quality of dietary protein on drug metabolism. 97 91

We assessed the growth rate and changes in plasma albumin, total protein and alpha 2-macroglobulin concentrations (a major acute phase protein in rats) before and after a subcutaneous injection of turpentine (0.5 mg/kg body wt) in groups of rats receiving one of a series of protein-deficient diets (protein concentrations of 0.5, 1.5, 3.0, 4.5 or 6.0 g/100 g) or a diet containing an adequate level of protein (20 g/100 g) for maximal growth. Increasing protein deficiency in the different groups of animals reduced the basal albumin and total protein concentrations and attenuated the total protein and alpha 2-macroglobulin responses to turpentine. Increasing protein deficiency delayed the time taken for alpha 2-macroglobulin to reach peak concentrations post-injection and its return to basal concentrations. The turpentine-induced hypoalbuminemia was similar in all groups of animals (approximately 10 g/L depression) but restoration to values that were present before turpentine injection was increasingly delayed with increasing protein deficiency. The magnitude of the acute phase response (peak alpha 2-macroglobulin concentration) was found to be directly related to growth rate (r = 0.70, P less than 0.001). We concluded that protein deficiency can alter the pattern and magnitude of the acute phase responses in circulating protein concentrations to an extent that is dependent on the severity of protein deficiency.
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PMID:The magnitude of the acute phase protein response is attenuated by protein deficiency in rats. 137 88

Adult rats, submitted from gestation to the basic regional diet (BRD) of some human populations in the northeastern region of Brazil, presented higher velocities of propagation of cortical spreading depression (SD) than well-nourished animals. This effect was also seen in rats receiving BRD during the gestation and suckling periods alone but not when this diet was administered only during adult life, suggesting that the alterations produced by BRD occur early in life. The supplementation of BRD with lipids, vitamins and minerals (but not protein) did not prevent the appearance of this facilitatory effect in the gestation + suckling group, suggesting an important effect of protein deficiency in the BRD on cortical SD.
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PMID:Propagation of cortical spreading depression in malnourished rats: facilitatory effect of dietary protein deficiency. 345 58

Two groups of guinea pigs were maintained on high-protein and low-protein diets and immunized with intradermal BCG. Protein deficiency was accompanied by marked inhibition of local and systemic immune responses: a) The BCG nodule was poorly formed. There was marked delay and deficiency in the mobilization of macrophages. b) The draining lymph node was atrophic and showed little or no proliferation of lymphoid cells in the paracortical area. Macrophage accumulation occurred late but became diffuse and marked, in contrast to its consistent scarcity in the BCG nodule. c) In either location epithelioid cell transformation was retarded. Well-formed mature epithelioid cell granulomas were not seen. d) Bacilli persisted for a long time in the skin and lymph node lesions, e) Tuberculin sensitivity was greatly impaired in one-fifth of animals and absent in others. These findings were suggestive of macrophage dysfunction and depression of cell-mediated immunity to BCG in the protein-deficient guinea pig.
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PMID:Immune responses of the protein-deficient guinea pig to BCG vaccination. 472 96

The course of parasitaemia and certain immune responses in protein or calorie-deficient albino rats infected with Plasmodium berghei (NICD) were studied. Wide variations observed in the course of parasitaemia in protein-deficient animals were (a) prolonged prepatent period, short patent period with low parasitaemia (50% of animals), (b) short prepatent period and an inability to resolve the infection (14% of animals) and (c) no patent parasitaemia at any stage of observation (23.5% of animals). The calorie-deficient animals had significantly lower parasitaemia (P less than 0.05) compared with well fed animals. Protein deficiency resulted in depression of T-dependent immune responses in uninfected as well as P. berghei-infected animals. The outcome of the parasitaemia in protein- as well as calorie-deficient animals seems to be the combined result of deficiencies of certain essential nutrients, proteins and calories in the diet as well as the immune responses of the host.
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PMID:Interactions of protein calorie malnutrition, malaria infection and immune responses. 641 16

The influence of protein deficiency was evaluated on immune responsiveness after subchronic DDT exposure in albino rats. Rats were given 20%, 12% and 3% protein diets and exposed to DDT (20, 50 or 100 ppm) for 4 weeks. DDT (50 and 100 ppm) induced humoral and cellular immune suppression only in rats fed on 3% protein diet. There was (a) an increase in the albumin/globulin ratio, (b) suppression in IgM and IgG levels, and (c) attenuation in the tetanus toxoid-induced antibody responses. Further, in rats immunized with tetanus toxoid, the leucocyte and macrophage migration inhibition were also attenuated. Moreover, these animals maintained on 3% protein diet showed depression in humoral and cellular immune responses to antigen in a dose-dependent pattern after exposure to DDT at dose levels which were not immunosuppressive for rats on 12% or 20% protein diet. These results suggest that dietary protein content may predispose to the immunotoxic effects of DDT exposure, and also be a crucial determinant in DDT detoxification.
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PMID:Influence of dietary protein on DDT-induced immune responsiveness in rats. 857 4

We examined whether vitamin A improved mucosal immune depression in mice with wasting protein deficiency. In male C3H/HeN mice fed a semi-purified 1% protein diet for 2 wk, plasma retinol and immunoglobulin A (IgA) concentrations in the small intestinal mucosa were 50 and 55%, respectively, of those in mice fed a semi-purified 20% protein diet, (P < 0.05). Daily supplementation of 0.3 mg of retinyl acetate to protein-deficient mice for 2 wk increased the plasma retinol level to the value in the protein-sufficient mice. However, 1 mg/d of retinyl acetate was required to prevent the decline of the IgA level caused by the protein deficiency. Mice fed the low-protein diet had lower concentrations of IL-4 and IL-5 in the small intestinal mucosa and fewer IL-4- and IL-5-containing cells in the lamina propria (P < 0. 05). Retinyl acetate (1 mg) significantly restored the IL-5 level and the number of IL-4- and IL-5-containing cells. After immunization with 20 microg of cholera toxin (CT), the intestinal mucosa of protein-deficient mice contained significantly less CT-specific IgA than control mice. Treatment with 1 mg of retinyl acetate prevented the decline of anti-CT IgA level in the protein-deficient mice, improving their survival rate after an exposure to 0.1 mg of CT. These results suggest that large oral supplements of vitamin A may preserve mucosal IgA level during protein malnutrition, possibly by stimulating Th2 cytokine production and thereby, inducing resistance against infection.
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PMID:Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levels in small intestinal mucosa of protein-malnourished mice. 1022 82

Dietary protein deficiency, common in elderly, is associated with decreased areal bone mineral density and plasma insulin-like growth factor I (IGF-I). To investigate the early adaptation of bone cells to protein restriction, 6-month-old female rats were pair-fed with isocaloric 15% (control) or 2.5% casein diets for 14 days. Animals were then treated daily with rhIGF-I/IGFBP-3 (1:4, 2.5 mg IGF-I/kg BW) or with vehicle for 10 days. After double-labeling, proximal metaphysis and mid-diaphysis of the tibia were analyzed histomorphometrically. Plasma osteocalcin, IGF-I, and urinary deoxypyridinoline were quantified. After 14 days of protein restriction, significant drops in plasma osteocalcin (13%) and IGF-I (37%), in periosteal formation (83%) and mineral apposition (49%) rates are observed, indicating a decreased osteoblast recruitment and activity. In cancellous bone, a significant decrease in active eroded surfaces (27%) and osteoclast number (24%) indicates a transient depression of resorption. In rats fed the 15% casein diet, rhIGF-I/IGFBP-3 increases cancellous (42%) and periosteal (600%) formation rates, indicating an increased osteoblast recruitment. In protein-restricted rats, rhIGF-I/IGFBP-3 fails to increase cancellous or periosteal bone formation and plasma osteocalcin is significantly lower than in 15% casein+rhIGF-I/ IGFBP-3 rats. Protein restriction induces osteoblast resistance to rhIGF-I/IGFBP-3 in both bone envelopes. Low plasma IGF-I and osteoblast resistance to IGF-I, may contribute to the impaired periosteal formation.
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PMID:Dietary protein restriction lowers plasma insulin-like growth factor I (IGF-I), impairs cortical bone formation, and induces osteoblastic resistance to IGF-I in adult female rats. 1096 85


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