scholarly journals Effects of sublethal doses of gossypol on haematological properties and biochemical metabolites of male rabbit

2019 ◽  
Vol 27 (4) ◽  
pp. 237
Author(s):  
T.A. Ramadan ◽  
A.M. Rashad

The purpose of this study was to investigate the effects of two sublethal doses of gossypol (GOS) (4 and 20 mg/kg of body weight), administered every other day, on some haematological, biochemical, enzymatic and electrolytic properties and amino and fatty acids in male rabbit blood plasma. The experiment lasted for 16 wk and included two phases: 1) administration period; rabbits were given the experimental doses of GOS for 8 wk; and 2) recovery period; rabbits were allowed 8 wk for complete withdrawal of drugs from the plasma. Results showed that low levels of gossypol increased (<em>P</em>&lt;0.01) haemoglobin, mean corpuscular haemoglobin and white blood cells compared to control. Plasma total protein was increased (<em>P</em>&lt;0.01) by the low GOS dose in both experimental phases. Likewise, glucose concentration was increased (<em>P</em>&lt;0.01) by the high GOS dose during the recovery period. Aspartate aminotransferase and alanine aminotransferase enzymes were increased (<em>P</em>&lt;0.01) by the high dose of GOS treatment only. Low GOS dose increased (<em>P</em>&lt;0.01) blood plasma Na+ concentration in the recovery period only. Results revealed that total essential amino acids (EAA), and EAA/non-EAA ratio were not affected in a dose-dependent manner during the treatment phase expect for plasma proline, which was increased along with non-EAA (<em>P</em>&lt;0.01) by high GOS dose. Additionally, GOS administration did not affect total unsaturated fatty acids (USFA), total saturated fatty acids (SFA) and SFA/USFA ratio in a dose-dependent manner. In conclusion, Gossypol treatment affected rabbit haematological parameters and biochemical properties of blood plasma in a dose-dependent manner.

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Hojun Lee ◽  
Jae-Young Lim ◽  
Seung-Jun Choi

Accumulation of saturated fatty acids contributes to lipotoxicity-related insulin resistance and atrophy in skeletal muscle. Conversely, unsaturated fatty acids like docosahexaenoic acid were proven to preserve muscle mass. However, it is not known if the most common unsaturated oleate will protect skeletal myotubes against palmitate-mediated atrophy, and its specific mechanism remains to be elucidated. Therefore, we investigated the effects of oleate on atrophy-related factors in palmitate-conditioned myotubes. Exposure of myotubes to palmitate, but not to oleate, led to an induction of fragmented nuclei, myotube loss, atrophy, and mitochondrial superoxide in a dose-dependent manner. Treatment of oleate to myotubes attenuated production of palmitate-induced mitochondrial superoxide in a dose-dependent manner. The treatment of oleate or MitoTEMPO to palmitate-conditioned myotubes led to inhibition of palmitate-induced mRNA expression of proinflammatory (TNF-αand IL6), mitochondrial fission (Drp1 and Fis1), and atrophy markers (myostatin and atrogin1). In accordance with the gene expression data, our immunocytochemistry experiment demonstrated that oleate and MitoTEMPO prevented or attenuated palmitate-mediated myotube shrinkage. These results provide a mechanism indicating that oleate prevents palmitate-mediated atrophy via at least partial modulation of mitochondrial superoxide production.


1982 ◽  
Vol 242 (4) ◽  
pp. H629-H632
Author(s):  
W. I. Rosenblum

Cerebral surface arterioles of the mouse were constricted in a dose-dependent manner by three different unsaturated fatty acids each with one of its double bonds in the n-6 position: arachidonate, linoleic, and 11,14,17-eicosatrienoic acid (ETA) in doses of 10-200 micrograms/ml. The constriction was transient, and its magnitude was significantly reduced by pretreatment of the mice with intraperitoneal injections of indomethacin (5 mg/kg), aspirin (100 mg/kg), or sodium 2-amino-3-(4 chlorobenzyl)-phenylacetate (AHR-6293, 100 mg/kg). The inhibitory effect of these cyclooxygenase inhibitors suggests that this enzyme is involved in the response to these fatty acids and is in keeping with suggestions in the literature stating that such unsaturated fatty acids may interact with cyclooxygenase even when they cannot form prostaglandin (PG) endoperoxides, The PG endoperoxide formed by arachidonate or the analogous hydroperoxy compounds formed by linoleic or 11,14,17 ETA, may then alter cerebrovascular tone by production of reactive, O2-containing species. Alternate explanations for the data are also proposed.


1984 ◽  
Vol 218 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Y Fujimoto ◽  
N Akamatsu ◽  
A Hattori ◽  
T Fujita

We have investigated the effects of phospholipase A2 and C on the synthesis of prostaglandin E2 in rabbit kidney medulla and the release of fatty acids from the medulla slices. Exogenous phospholipase A2 [from Naja naja (Indian cobra) venom] and phospholipase C (from Clostridium welchii) stimulated prostaglandin E2 production in a dose-dependent manner. At the maximal effective concentrations (0.5 unit of phospholipase A2/ml, 2 units of phospholipase C/ml), phospholipase C increased prostaglandin E2 formation to the level observed with phospholipase A2. Phospholipase A2 enhanced the release only of unsaturated fatty acids, whereas phospholipase C stimulated the release of individual free fatty acids (C 16:0, C 18:0, C 18:1, C 18:2 and C 20:4). Moreover, p-bromophenacyl bromide inhibited phospholipase A2-stimulated prostaglandin E2 production and the release of fatty acids, but it had no influence on prostaglandin E2 formation and the release of fatty acids increased by phospholipase C, indicating that the stimulatory effect of phospholipase C is not mediated through the activation of endogenous phospholipase A2. These results suggest the presence of diacylglycerol lipase and monoacylglycerol lipase in the kidney and the importance of this pathway in prostaglandin synthesis by the kidney.


1991 ◽  
Vol 260 (3) ◽  
pp. C439-C448 ◽  
Author(s):  
J. M. Burt ◽  
K. D. Massey ◽  
B. N. Minnich

The permeability and conductance of gap junctions between pairs of neonatal rat heart cells were rapidly and reversibly decreased by oleic acid in a dose- and time-dependent manner. Other unsaturated fatty acids (C-18: cis 6, 9, or 11, and C-18, 16, and 14, cis 9), saturated fatty acids (C-10, 12, and 14), and saturated fatty alcohols (C-8, 10, and 12) also caused uncoupling. The most effective compounds of the unsaturated and saturated fatty acid and saturated fatty alcohol series caused essentially complete uncoupling at comparable aqueous concentrations. However, oleic acid uncoupled cells at membrane concentrations as low as 1 mol%, whereas decanoic acid required upwards of 35 mol%. The channels that support the action potential remained functional at these same membrane concentrations. The data are discussed in terms of the possible mechanism by which these compounds cause uncoupling and the possible role of uncoupling by nonesterified free fatty acids in the initiation of arrhythmias during and after ischemic insults.


2021 ◽  
Vol 12 (4) ◽  
Author(s):  
I. A. Hryshchuk ◽  
◽  
V. I. Karpovskyi ◽  
V. V. Danchuk ◽  
B. V. Gutyj ◽  
...  

Coordination of physiological activity and intensity of metabolism in various organs and tissues of a productive animal, depending on environmental conditions and own needs, is provided by the regulatory activity of the corresponding nerve centers. However, the features of the autonomic regulation of the nervous system in this matter can have a significant impact not only on the physiological activity of animals but also on their productivity. Therefore, the question of studying the influence of autonomic regulation on the animal body in general and the interaction of the autonomic system and lipid metabolism is quite relevant. Groups of animals were formed by determining the state of the cardiovascular system according to Baevskyi. Blood plasma was used for the study, lipid extraction was performed by the Folch method. Fatty acid analysis was performed on a Trace GC Ultra gas chromatograph (USA) with a flame ionization detector. Studies have shown that the relative content of saturated fatty acids in blood of normotonics was the highest compared with other groups: sympathotonics – by 1.9%; vagotonics – 0.48%. Regarding the concentration of saturated fatty acids in sympathotonics, it should be noted that the content of stearic acid was the highest (18.07 ± 0.01; P < 0.001) and saturated fatty acids from C6 to C16 were characterized by the lowest values (P < 0.01–0.05) in comparison with other groups The total content of unsaturated fatty acids in blood plasma of sympathotonics and vagotonics was 1.19% and 0.49% higher, respectively, compared with normotonics. Quite interesting is the fact that sympathotonics were characterized by the highest content of polyunsaturated fatty acids, the content of which decreased in the range C18:2n6 > C20:4n6 > C18:3n3 > C22:6n3 > C22:5n3, a similar sequence we observed in other groups, although the relative concentration of acids could fluctuate. Normotonics were characterized by the highest levels of some polyunsaturated fatty acids (C18:3n3, C22:5n3, C22:6n3) (P < 0.05-0.01), while levels of some unsaturated fatty acids (C18: 1n9, C20: 3n6) were the lowest. Thus, the type of nervous activity has a significant effect on the ratio of fatty acids in blood plasma of cows and autonomous regulation affects the metabolic processes in the animal’s body.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Bo Gao ◽  
Qiang Huang ◽  
Qiang Jie ◽  
Wei-Guang Lu ◽  
Long Wang ◽  
...  

Abstract Free fatty acids display diverse effects as signalling molecules through GPCRs in addition to their involvement in cellular metabolism. GPR120, a G protein-coupled receptor for long-chain unsaturated fatty acids, has been reported to mediate adipogenesis in lipid metabolism. However, whether GPR120 also mediates osteogenesis and regulates BMMSCs remain unclear. In this study, we showed that GPR120 targeted the bi-potential differentiation of BMMSCs in a ligand dose-dependent manner. High concentrations of TUG-891 (a highly selective agonist of GPR120) promoted osteogenesis via the Ras-ERK1/2 cascade, while low concentrations elevated P38 and increased adipogenesis. The fine molecular regulation of GPR120 was implemented by up-regulating different integrin subunits (α1, α2 and β1; α5 and β3). The administration of high doses of TUG-891 rescued oestrogen-deficient bone loss in vivo, further supporting an essential role of GPR120 in bone metabolism. Our findings, for the first time, showed that GPR120-mediated cellular signalling determines the bi-potential differentiation of BMMSCs in a dose-dependent manner. Additionally, the induction of different integrin subunits was involved in the cytoplasmic regulation of a seesaw-like balance between ERK and p38 phosphorylation. These findings provide new hope for developing novel remedies to treat osteoporosis by adjusting the GPR120-mediated differentiation balance of BMMSCs.


1986 ◽  
Vol 237 (3) ◽  
pp. 749-755 ◽  
Author(s):  
P L H Hwang

It is known that triphenylethylene anti-oestrogens such as tamoxifen bind to specific high-affinity anti-oestrogen-binding sites, which are distinct from oestrogen receptors. These binding sites are widely distributed in human and animal tissues, but their function and endogenous ligands are unknown. By using [3H]tamoxifen and a rat liver microsomal fraction, a radio-ligand-binding assay was developed in an attempt to identify endogenous ligands for the anti-oestrogen-binding sites in the rat. An ether extract of rat serum inhibited [3H]tamoxifen binding to rat liver binding sites in a dose-dependent manner. Identification of the active serum constituents that inhibited [3H]tamoxifen binding was achieved by g.l.c.-mass spectrometry after preliminary purification of a rat serum extract by silica-gel t.l.c. Three unsaturated fatty acids (oleic, linoleic and arachidonic) accounted for about 50% of the total inhibiting activity of the serum extract. The concentrations of these fatty acids required to inhibit [3H]tamoxifen binding were in the range of 10-100 microM, comparable with those found in the rat circulation under physiological conditions. Saturated fatty acids present in rat serum (palmitic and stearic) did not inhibit [3H]tamoxifen binding. A survey of other fatty acids revealed that, in general, unsaturated fatty acids were far more potent than saturated fatty acids in inhibiting [3H]tamoxifen binding. These studies demonstrate that unsaturated fatty acids are quantitatively the most important circulating inhibitors of [3H]tamoxifen binding to the anti-oestrogen-binding sites. The biological significance of their interaction with these sites, however, remains to be clarified.


2018 ◽  
Vol 63 (No. 6) ◽  
pp. 222-229
Author(s):  
M. Skřivan ◽  
M. Marounek ◽  
M. Englmaierová ◽  
E. Skřivanová ◽  
K. Růnová

The ileal digestibility of amino acids and fatty acids in young chickens fed control diet or experimental diets supplemented with freeze-dried pasture herbage at 20 or 40 g/kg was studied. Control diet contained wheat, maize, and soybean meal. Predominant species in the pasture herbage harvested in May were Lolium perenne, Festuca pratensis, and Trifolium pratense. Freeze-dried pasture herbage contained less protein (169 g/kg) and fat (24 g/kg) and more neutral detergent and acid detergent fibre (340 and 210 g/kg) and tannins (12.38 g/kg) than control diet. Concentrations of amino acids, except phenylalanine and threonine, were lower in pasture herbage than in control feed. In both the control feed and freeze-dried pasture herbage, unsaturated fatty acids occurred in higher proportions than saturated fatty acids. In freeze-dried pasture herbage linolenic acid was the main fatty acid. In chickens fed freeze-dried pasture herbage the ileal digestibility of amino acids and fatty acids decreased in a dose-dependent manner. Freeze-dried pasture herbage at 4% in diet had negative effect (P &lt; 0.05) on the digestibility of amino acids and fatty acids in comparison with control diet. But there was no significant effect of 2% freeze-dried pasture herbage in diet on amino acids digestibility. This suggests that pasture herbage contains anti-nutritional factors that inhibit proteolysis and lipolysis. The effect of pasture herbage on digestibility was variable. In chickens fed diets containing 4% freeze-dried pasture herbage, apparent ileal digestibility of amino acids varied from 0.39 (cysteine) to 0.91 (methionine). Variability in the ileal digestibility of fatty acids was less pronounced (from 0.65 to 0.89).


2001 ◽  
Vol 56 (1-2) ◽  
pp. 111-121 ◽  
Author(s):  
Meinrad Boll ◽  
Lutz W. D. Weber ◽  
Eberhard Becker ◽  
Andreas Stampfl

Abstract The CCl4-induced development of liver damage was studied in monolayer cultures of pri­mary rat hepatocytes: (1) CCl4 caused accumulation of triglycerides in hepatocytes following cytochrome P450 induction with β-naphthoflavone or metyrapone. Ethanol or a high dose of insulin plus triio­dothyronine had the same effect. (2) CCl4 increased the synthesis of fatty acids and triglycer­ ides and the rate of lipid esterification. Cholesterol and phospholipid synthesis from acetate was also increased. (3) CCl4 reduced β-oxidation of fatty acids as assessed by CO2-release and ketone body formation. Hydrolysis of triglycerides was also reduced. (4) The content of unsaturated fatty acids in microsomal lipids was decreased by almost 50% after incubation with CCl4, while saturated fatty acids increased slightly. (5) CCl4 exerted a pronounced inhibitory effect on the exocytosis of macromolecules (albumin), but did not affect secretion of bile acids from hepatocytes.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Christopher T. Migliaccio ◽  
Raymond F. Hamilton ◽  
Pamela K. Shaw ◽  
Joseph F. Rhoderick ◽  
Sanghamitra Deb ◽  
...  

Abstract Background A very pure multi-walled carbon nanotube (MWCNT) that was shown to have very low toxicity in vitro, was evaluated for lung and systemic effects and distribution following inhalation exposure. Methods B6C3F1/N mice were exposed to varying doses (0, 0.06, 0.2, and 0.6 mg/m3) of the (99.1% carbon) MWCNT by inhalation for 30 days (excluding weekends). Ten days following the last exposure, the lungs and spleen were harvested and processed for histology and immune cell population assessment. In addition, lung lavage cells and fluid were analyzed. Stimulated Raman scattering (SRS) was used to identify particles in the lungs, spleen, kidneys, liver, mediastinal and brachial lymph nodes, and olfactory bulb. Splenic tissue sections were stained with hematoxylin and eosin (H&E) for light microscopic histopathology assessment. Blood plasma was analyzed for cytokines and cathepsins. A section of the spleen was processed for RNA isolation and relative gene expression for 84 inflammation-related cytokines/chemokines. Results Following MWCNT exposure, particles were clearly evident in the lungs, spleens, lymph nodes and olfactory bulbs, (but not livers or kidneys) of exposed mice in a dose-dependent manner. Examination of the lavaged lung cells was unremarkable with no significant inflammation indicated at all particle doses. In contrast, histological examination of the spleen indicated the presence of apoptotic bodies within T cells regions of the white pulp area. Isolated splenic leukocytes had significant changes in various cells including an increased number of proinflammatory CD11b+Ly6C+ splenic cells. The gene expression studies confirmed this observation as several inflammation-related genes were upregulated particularly in the high dose exposure (0.6 mg/m3). Blood plasma evaluations showed a systemic down-regulation of inflammatory cytokines and a dose-dependent up-regulation of lysosomal cathepsins. Conclusions The findings in the lungs were consistent with our hypothesis that this MWCNT exposure would result in minimal lung inflammation and injury. However, the low toxicity of the MWCNT to lung macrophages may have contributed to enhanced migration of the MWCNT to the spleen through the lymph nodes, resulting in splenic toxicity and systemic changes in inflammatory mediators.


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