Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.
Two experiments were conducted to evaluate the effect of mold inhibitor in the ration which had two different protein levels (18% and 12%) and two different particle sizes (80 or 40% of the particles in the ration less than 1.19 mm). The experimental diets with ave. 12.7% moisture which were treated at the level of 0.1% mold inhibitor were stored under 85% humidity and at $29{\pm}1^{\circ}C$ for 10 to 40 days. In experiment 1, after 40 days of storage the $CO_2$ production in the feed treated with mold inhibitor was higher (p < 0.01) than when 40% of the ration's panicle size was 1.19 mm. Aflatoxin production in the experimental diet with mold inhibitor was affected (p<0.05) by the levels of protein and the different particle size ranges after 40 days storage. The interaction of protein levels and particle size ranges on the anatoxin and $CO_2$ production was significant (p<0.05) at 40 days storage. In experiment 2, there was a decrease in total body weight gain and total feed intake observed in chicks fed the untreated diet of 18% protein with 40% of the particles in the ration less than 1.19 mm stored for 40 days. Feed conversion was depressed (p<0.05) in the chicks fed the untreated diets of both particle sizes. Particle size X types of feed interaction in feed conversion was significant (p<0.05).
Intestinal phosphate (Pi) absorption across the apical membrane of small intestinal epithelial cells is mainly mediated by the type IIb Na-coupled phosphate co-transporter (NaPi-IIb), but its expression and regulation in the chicken remain unclear. In the present study, we investigated the mRNA and protein levels of NaPi-IIb in three regions of chicken small intestine, and related their expression levels to the rate of net phosphate absorption. Our results showed that maximal phosphate absorption occurs in the jejunum, however the highest expression levels of NaPi-IIb mRNA and protein occurs in the duodenum. In response to a low-Pi diet (TP 0.2%), there is an adaptive response restricted to the duodenum, with increased brush border membrane (BBM) Na-Pi transport activity and NaPi-IIb protein and mRNA abundance. However, when switched from a low-(TP 0.2%) to a normal diet (TP 0.6%) for 4 h, there is an increase in BBM NaPi-IIb protein abundance in the jejunum, but no changes in BBM NaPi-IIb mRNA. Therefore, our study indicates that Na-Pi transport activity and NaPi-IIb protein expression are differentially regulated in the duodenum vs the jejunum in the chicken.
Male germ cell apoptosis has been extensively explored in rodent. In contrast, very little is known about their susceptibility to apoptosis stimuli of developing germ cell stages at the time when germ cell depletion after busulfan treatment occurs. Furthermore, it is still unanswered how spermatogonial stem cells are resistant to busulfan treatment. We examined the change of gene expression in detail using cDNA microarray analysis of mouse testis treated with busulfan. A subtoxic dose of busulfan (40mg/kg of body weight) transiently increased 228 mRNA levels among of the 8000 genes analyzed. TagMan analysis confirmed that the mRNA levels such as defensive protein, support protein, enzymatic protein, transport protein, and hormonal protein were rapidly increased. These results were re-confirmed by real-time PCR analysis. However, the expression levels of these genes induced by busulfan treatment were significantly reduced in control testis, indicating that both of male germ cells and somatic cells after busulfan treatment induces self-defense mechanism for protection of testicular cell death. Among them, we conclude that defense proteins play a key role in testis injury induced by busulfan.
An ABC transporter apparatus of the Gram-negative bacterial type I secretion pathway can be used as a secretory protein expression system in Escherichia coli. Four types of coexpression systems for the Pseudomonas fluorescens lipase gene, tliA, and its cognate ABC transporter gene cluster, tliDEF, were constructed. When the relative expression levels were changed by adding different concentrations of IPTG, the secretion (16.9 U/ml of culture) of TliA in E. coli [pTliDEFA-223+pACYC184] was significantly higher than E. coli [pKK223-3+pTliDEFA-184] secreting the lowest level of TliA (5.2 U/ml of culture). Maximal accumulation of the lipase secreted occurred in the mid-exponential phase, implying that the efficient protein secretion via an ABC transporter was restricted only to actively growing cells. Finally, the secretion level of TliA in E. coli [pTliDEFA-223+pACYC184] was increased to 26.4 U/ml by inducing gene expression at the culture initiation time. These results indicate that a significant increase in the ABC transporter-dependent protein secretion can be achieved by simply controlling the relative expression levels between the ABC transporter and its passenger protein, even in the recombinant E. coli cells.
This experiment was conducted to study the sparing effects of animal proteins on weight gain, nutrients utilizability and economic analysis of broiler. Experiment diet contained different ratio of animal and plant protein and were supplemented different levels of methionine and lysine for the respective protein levels. A total of 264 broiler chicks were fed four diets of control, $T_1$, $T_2$ and $T_3$ for 42 days from April 7, 1990 to May 19, 1990. Dietary protein levels of control, $T_1$, $T_2$ and $T_3$ for starter and finisher were 20~18, 18~16, 18~16 and 22~20%, respectively. Methionine and lysine levels of control, $T_1$, $T_2$ and $T_3$ were 0.4~1.1, 0.44~1.21, 0.48~1.32 and 0.48~1.32% for starter diet, respectively, and were 0.32~0.90. 0.35~0.99, 0.38~1.08 and 0.38~1.08% for finisher diet, respectively. The results obtained were summarized as follows. 1. The birds fed control diet gained most for overall period. $T_3$ treatment which was high in protein, methionine and lysine levels gained most for finisher period. 2 The birds fed control diet consumed most feed, and the birds fed T$_3$ diet consumed least feed. for overall period. Feed conversion during 1~4 weeks was better in $T_1$ (1.51) and $T_2$ (1.53) than in control (1.61) and $T_3$ (1.63) . During 4~6weeks, feed conversion was better in $T_3$ (1.37) and control(1.58) than T, (2.05) and T, (2.16) (P<0.01) 3. Dry matter, crude fiber and NFE utilizability were increased for 1~4 weeks and decreased for 4~6 weeks as methionine and lysine levels increased and crude protein utilizability tended to be increased as protein levels increased. 4. Abdominal fat content was lowest in bird fed control diet and was high in birds fed low protein diet Carcass percentage was highest at control and the abdominal fat content was higher in bird fed lower protein diet than bird fed other protein diets(P<0.05). 5. Feed cost per kg weight gain was lowest at $T_3$ which contained more soybean oil meal than other feeds and next was control. According to the results of this experiment, it was revealed that optimum protein, methionine and lysine levels for starter and finisher broiler diet were 20~18, 0.4~0.32 and 1.1~0.9%, respectively.
It has been demonstrated that vanadate causes nephrotoxicity. Vanadate inhibits renal sodium potassium adenosine triphosphatase (Na, K-ATPase) activity and this is more pronounced in injured renal tissues. Cardiac cyclic adenosine monophosphate (cAMP) is enhanced by vanadate, while increased cAMP suppresses Na, K-ATPase action in renal tubular cells. There are no in vivo data collectively demonstrating the effect of vanadate on renal cAMP levels; on the abundance of the alpha 1 isoform (${\alpha}_1$) of the Na, K-ATPase protein or its cellular localization; or on renal tissue injury. In this study, rats received a normal saline solution or vanadate (5 mg/kg BW) by intraperitoneal injection for 10 days. Levels of vanadium, cAMP, and malondialdehyde (MDA), a marker of lipid peroxidation were measured in renal tissues. Protein abundance and the localization of renal ${\alpha}_1-Na$, K-ATPase was determined by Western blot and immunohistochemistry, respectively. Renal tissue injury was examined by histological evaluation and renal function was assessed by blood biochemical parameters. Rats treated with vanadate had markedly increased vanadium levels in their plasma, urine, and renal tissues. Vanadate significantly induced renal cAMP and MDA accumulation, whereas the protein level of ${\alpha}_1-Na$, K-ATPase was suppressed. Vanadate caused renal damage, azotemia, hypokalemia, and hypophosphatemia. Fractional excretions of all studied electrolytes were increased with vanadate administration. These in vivo findings demonstrate that vanadate might suppress renal ${\alpha}_1-Na$, K-ATPase protein functionally by enhancing cAMP and structurally by augmenting lipid peroxidation.
Journal of the Korean Society of Food Science and Nutrition
/
v.19
no.1
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pp.27-34
/
1990
This study was undertatken to investigate the effects of dietary vitamin E on the toxicity of cadmium(Cd) in rats. The two variables were the supplmentary vitamin E(400lU/kg) and the protein amount(10.5% in the low protein diet and 18.0% in the normal protein diet) In cadmium treated rats net weight gain and food intake were decreased but improved by supplementation with vitamin E in the normal protein, hematocrit values reduced by Cd were significantly increased by the addition of vitamin E to normal protein diet in Cd intoxicated rats, The supplementation with vitamin E diminished the effect of Cd on aspartate aminotransf-rase and alanine aminotransferase activities in serum In Cd treated rats fed normal protein diet with vitamin E the contents of triglyceride were decreased and total-cholesterol contents were significantly reduced in serum and both of them in liver were markedly decreased. The activity of alcohol dehydrogenase in liver was decreased by Cd however supplementation with vitamin E reduced the effects of Cd on hepatic alcohol dehydrogenase. the results of this experiment indicated that there was some interaction between vitamin E and protein levels and supplementation with vitamin E had an effect more than protein levels oncd toxicity.
The climate and marketing system of raw milk in Taiwan create problems in balance feeding of protein and energy in lactating cows in Taiwan. Level of urea nitrogen both in bulk milk and serum reflects ruminal protein degradation and post-ruminal protein provision, whereas milk protein concentration responds to dietary energy intake and bacterial protein production in the rumen. Establishment of a range of reference standards in milk protein and urea nitrogen levels can be applied as a noninvasive economical feeding guide to monitor the balance of protein and energy intake. Standard reference levels of 3.0% milk protein and 11-17 mg/dL milk urea nitrogen (MUN) were established. Level of milk protein below 3.0% is regarded as indicating inadequate dietary energy whereas MUN below or above the range is regarded as a deficiency or surplus in dietary protein. Results from analysis of bulk a milk samples collected from 174 dairy herds over Taiwan showed that only one quarter (25.29%) of the herds received a balanced intake of protein and energy, 33.33% adequate protein with energy inadequate, 22.99% herds in protein surplus with energy inadequate, 10.35% herds in protein surplus with energy adequate, 4.6% protein deficiency with energy adequate, and 3.45% herds with both protein and energy inadequate. Energy inadequate herds accounted for 60% of the total dairy herds in Taiwan with 56% adequate, 38% surplus and 6% inadequate in protein. In comparing milk sampled from bulk milk on different seasons from Lee-Kang area in the southern Taiwan, the concentrations of milk fat and milk protein were significantly higher in the cool season (February) than in the warm season (August) (p<0.05), whereas the urea nitrogen in the milk was significantly lower in the cool season than in the warm season (p<0.05). This indicated that lactating cows had excess protein and/or inadequate energy intake in the warm season in this area. It appears that the major problem feeding in lactating cows is energy intake shortage, especially during the warm season in Taiwan.
Kim, S.W.;Han, I.K.;Choi, Y.J.;Kim, Y.H.;Shin, I.S.;Chae, B.J.
Asian-Australasian Journal of Animal Sciences
/
v.8
no.5
/
pp.463-470
/
1995
An experiment was conducted to evaluate the effects of chromium picolinate on growth performance, nutrient utilizability, carcass composition, serum traits and in vitro protein synthesis of 3 day old Arbor Acres broiler chickens when dietary crude protein levels were varying in diets. Six replicates of eight chicks each (average initial weitht = 59.4 g) were randomly assigned to three levels (low, medium, high) of dietary crude protein at two levels of chromium (0, 200 ppb Cr/kg diet) as chromium picolinate. Six chicks/treatment were randomly chosen for analyses of carcass composition, six additional chicks/treatment were randomly chosen for analyses of serum components, and a chick/treatment was chosen for in vitro culture of liver tissue. Chromium picolinate did not affect feed intake, protein and fat utilizability, regradless of dietary crude protein level. But feed/gain ratio were more improved in groups fed the low protein diets added with chromium picolinate compared with groups fed the medium and high protein diets with chromium picolinate. Carcass fat tended to decrease whereas carcass protein tended to increase when added with chromium picolinate. Broilers fed diets with chromium picolinate exhibited lower serum triglyceride and nonesterified fatty acid concentrations than those fed without chromium picolinate (p < 0.05). Both secreted and retained proteins in cultured acinar cell were higher in groups fed diets with chromium picolinate than those fed diets without chromium picolinate (p < 0.05). It could be suggested that chromium picolinate was effective in improving weight gain and nutrient utilizability when dietary crude protein was low (p < 0.05), and also effective in manipulating carcass fat when dietary crude protein level was high (p < 0.05).
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