seeds of Pisum sativum
L-(-)-Carnitine/karnitin/ST 198/3-Carboxy-2-hydroxy-N,N,N-trimethyl-1-propanaminium Hydroxide Inner Salt/Carnitrine/USPorFCC/(R)-Carnitine/Ammonium, (3-carboxy-2-hydroxypropyl)trimethyl-, hydroxide, inner salt, L-/L-CARNITIN/3-Hydroxy-4-(trimethylammonio)butanoate/g-Trimethylammonium-b-hydroxybutirate/CAR-OH/Vitamin BT/Monocamin/1-Propanaminium, 3-carboxy-2-hydroxy-N,N,N-trimethyl-, inner salt/(-)-Carnitine/Carnitene/DL-Carnitine/(-)-(R)-3-Hydroxy-4-(trimethylammonio)butyrate/carnitine (L-form)/(R)-3-Carboxy-2-hydroxy-N,N,N-trimethyl-1-propanaminium hydroxide inner salt/γ-Trimethyl-β-hydroxybutyrobetaine/Carnitine, (-)-/1-Propanaminium, 3-carboxy-2-hydroxy-N,N,N-trimethyl-, inner salt, (2R)-/(R)-3-hydroxy-4-(trimethylammonio)butanoate/(-)-L-Carnitin/L(-)-Carnitine/Carnitine, L-/3-Hydroxy-4-trimethylammoniobutanoate/(L-3-Carboxy-2-hydroxypropyl)trimethylammonium hydroxide inner salt/Carnitine DL-form/L-Carnitine/BICARNESINE/Cardiogen/4-Copab/L-Carnitine inner salt/g-Trimethyl-b-hydroxybutyrobetaine/(3R)-3-Hydroxy-4-(trimethylammonio)butanoate/Levocarnitine/g-Amino-b-hydroxybutyric Acid Trimethylbetaine/(−)-(R)-3-Hydroxy-4-(trimethylammonio)butyrate/D,L-carnitine/(±)-carnitine/Carniking/carnitine/Carnitor
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provides coniferyl ferulate(CAS#:541-15-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
In mammals, the carnitine pool consists of nonesterified L-carnitine and many acylcarnitine esters. Of these esters, acetyl-L-carnitine is quantitatively and functionally the most significant. Carnitine homeostasis is maintained by absorption from diet, a modest rate of synthesis, and efficient renal reabsorption. Dietary L-carnitine is absorbed by active and passive transfer across enterocyte membranes. Bioavailability of dietary L-carnitine is 54-87% and is dependent on the amount of L-carnitine in the meal. Absorption of L-carnitine dietary supplements (0.5-6 g) is primarily passive; bioavailability is 14-18% of dose. Unabsorbed L-carnitine is mostly degraded by microorganisms in the large intestine. Circulating L-carnitine is distributed to two kinetically defined compartments: one large and slow-turnover (presumably muscle), and another relatively small and rapid-turnover (presumably liver, kidney, and other tissues). At normal dietary L-carnitine intake, whole-body turnover time in humans is 38-119 h. In vitro experiments suggest that acetyl-L-carnitine is partially hydrolyzed in enterocytes during absorption. In vivo, circulating acetyl-L-carnitine concentration was increased 43% after oral acetyl-L-carnitine supplements of 2 g/day, indicating that acetyl-L-carnitine is absorbed at least partially without hydrolysis. After single-dose intravenous administration (0.5 g), acetyl-L-carnitine is rapidly, but not completely hydrolyzed, and acetyl-L-carnitine and L-carnitine concentrations return to baseline within 12 h. At normal circulating l-carnitine concentrations, renal l-carnitine reabsorption is highly efficient (90-99% of filtered load; clearance, 1-3 mL/min), but displays saturation kinetics. Thus, as circulating L-carnitine concentration increases (as after high-dose intravenous or oral administration of L-carnitine), efficiency of reabsorption decreases and clearance increases, resulting in rapid decline of circulating L-carnitine concentration to baseline. Elimination kinetics for acetyl-L-carnitine are similar to those for L-carnitine. There is evidence for renal tubular secretion of both L-carnitine and acetyl-L-carnitine. Future research should address the correlation of supplement dosage, changes and maintenance of tissue L-carnitine and acetyl-L-carnitine concentrations, and metabolic and functional changes and outcomes.
Kinetics, pharmacokinetics, and regulation of L-carnitine and acetyl-L-carnitine metabolism.
To investigate the expression of the sperm-specific cation channel (CatSper1) in the epididymal sperm of varicocele (VC) rats and the effect of L-carnitine (LC) on the CatSper1 level.
Seventy male rats were equally randomized into groups A (normal control), B (VC model control), C (VC treated with normal saline), D (VC treated with low-dose LC), E (VC treated with medium-dose LC), F (VC treated with high-dose LC), and G (VC treated by prolonged medication of high-dose LC). The VC model was established by partial ligation of the left renal vein. At 12 weeks after modeling, the model rats in group C were treated intragastrically with normal saline at 1 ml/kg/d, those in groups D, E and F with LC at 0.05, 0.1 and 0.2 g/kg/d respectively, all for 5 consecutive weeks, and those in group G with LC at 0.2 g/kg/d for 7 successive weeks. Then, all the animals were sacrificed and their epididymides harvested for obtainment of the semen parameters by computer-assisted semen analysis (CASA) and determination of the mRNA and protein expressions of CatSper1 in the sperm by RT-PCR and Western blot.
Compared with the rats in group A, those in group B showed significantly decreased percentage of grade a+b sperm (P < 0.01), sperm viability (P < 0.01), sperm concentration (P < 0.01) and expressions of CatSper1 mRNA (1.44 ± 0.67 vs 0.71 ± 0.38, P < 0.01) and protein (1.87 ± 0.67 vs 0.84 ± 0.42, P < 0.01). In comparison with the animals in group C, those in the four LC intervention groups exhibited a markedly increased percentage of grade a+b sperm, sperm viability and mRNA and protein expressions of CatSper1, even more remarkably in groups F and G (P < 0.01). No statistically significant difference, however, was observed in sperm concentration between group C and the LC intervention groups (P > 0.05), nor in the mRNA and protein expressions of CatSper1 between groups F and G.
The expression of CatSper1 is decreased in the epididymal sperm of varicocele rats, and L-carnitine can increase the sperm viability, percentage of grade a+b sperm and CatSper1 expression of the rats.
L-carnitine ; rat; sperm; sperm-specific cation channel (CatSper1); varicocele
[Decreased expression of CatSper1 in the sperm of varicocele rats and protective effect of L-carnitine].
Wang SP1, Zhai YH2, Lu CM1, Cui YX1, Xu GY1, Wang XS3.
Neuro-schistosomiasis can induce neurological symptoms and severe disability. Since the resistance against the chemotherapy “praziquantel” was reported, the aim of the present study was investigating the anti-neuro-schistosomal effects of ZnO nanoparticles and/or L-carnitine (as free radicals scavenger) on schistosome-infected mice, where technology of nanoparticles has come to the forefront in the medical diagnosis and therapeutic drug delivery. In the human body, nanoscale-sized particles can move freely and reveal unique biological, mechanical, electrical, and chemical properties. In the present study, mice were divided into five groups. The first group served as the non-infected control group. Groups II, III, IV, and V were infected with cercariae of Schistosoma mansoni. Mice of groups III and IV were treated with ZnO nanoparticles (5.6 mg/kg b. wt.) and L-carnitine (500 mg/kg b. wt.), respectively, after 47 days post-infection. Finally, mice of the fifth group were injected with ZnO nanoparticles and after 1 h, the mice were intraperitoneally injected with L-carnitine once daily for 5 days. On day 52, post-infection mice of all groups were cervically decapitated. The treatment of ZnO nanoparticles and/or L-carnitine to schistosome-infected mice decreased brain oxidative stress parameters, where glutathione level and catalase activity were significantly increased as compared to schistosome-infected group. On the contrary, the treatment decreased nitrite/nitrate, malondialdehyde, and reactive oxygen species levels significantly. In addition, ZnO nanoparticles and/or L-carnitine treatment restored DNA laddering profile and improved the brain histopathological impairments resulting from neuro-schistosomiasis. Finally, the ZnO nanoparticle treatment and the co-treatment of ZnO nanoparticles and L-carnitine revealed anti-neuro-schistosomal effects on the infected mice.
DNA fragmentation; Histopathology; Mice; Neuro-schistosomiasis mansoni; Oxidative stress; ZnO nanoparticles
Zinc oxide nanoparticles and L-carnitine effects on neuro-schistosomiasis mansoni induced in mice.
2020 Mar 23
L-carnitine is constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias.Target: OthersL-Carnitine is an endogenous molecule involved in fatty acid metabolism, biosynthesized within the human body using amino acids: L-lysine and L-methionine, as substrates. L-Carnitine can also be found in many foods, but red meats, such as beef and lamb, are the best choices for adding carnitine into the diet . Administering L-carnitine (510 mg/day) to patients with the disease. L-carnitine treatment significantly improved the total time for dozing off during the daytime, calculated from the sleep logs, compared with that of placebo-treated periods. L-carnitine efficiently increased serum acylcarnitine levels, and reduced serum triglycerides concentration . L-carnitine and its derivatives show promise in the treatment of chronic conditions and diseases associated with mitochondrial dysfunction but further translational studies are needed to fully explore their potential .