Aspartate
Aspartic acid, also known as L-aspartate is a non-essential amino acid, which means that the body is able to manufacture its own supply. Besides, it is also the precursor of several amino acids, including four that are essential: methionine, threonine, isoleucine, and lysine. Aspartate promotes metabolism, and is used to treat fatigue and depression through its crucial role in generating cellular energy. Moreover, it is thought to boost the production of neurotransmitters and chemicals needed for normal mental functioning. Aspartate also strengthens the immune system by promoting the production of immunoglobulins and antibodies. It can quite easily be converted to glucose when demand for glucose exceeds supply. Aspartate also helps protect the liver by absorbing toxins and removing them from the bloodstream. It also protects the body from the effects of radiation. Good sources are sprouting seeds, oat flakes, wild game, avocado and asparagus. (For more detailed information, please visit ISM’s searchable database: Nutraceutical Search.)
Immune stimulators such as Corynebacterium parvum (CP) are useful for antitumoral and antiviral therapy. However, the immune trigger cannot be reactivated without adversely affecting the disease. We have tried to amplify the results yielded by a single injection of CP by using either interleukin-2 (IL2) or aspartate salts (ASP). In the present report, we show that IL2 has no detectable clinical effect. In contrast, the addition of an ASP salt increases the antiviral and antitumoral protection afforded by the CP-induced trigger. Moreover, treatment using only ASP slightly protects against tumor development and significantly increases antiviral resistance during experimental encephalomyocarditis (EMC) infection. This ASP-assisted CP immune stimulation improves antitumoral resistance even when ascitic tumors have already developed. In the latter case, tumor regression can even be detected. Since ASP increases T-cell cytotoxicity in vitro and aggravates spontaneous T-cell lymphomas in AKR mice, the involvement of T-cell-mediated immunity may explain antitumoral and antiviral effects. We propose the use of this therapeutic model for human cancer therapy, and possibly for treating AIDS.
o Chany, C, & Cerutti, I. (1986). Aspartate-assisted immune stimulation: its importance in antitumor and antiviral protection. Int J Cancer, 38(2), 159-64.
Transport systems specific for L-glutamate and L-aspartate play an important role in the termination of neurotransmitter signals at excitatory synapses. We describe here the structure and function of a 66-kDa glycoprotein that was purified from rat brain and identified as an L-glutamate/L-aspartate transporter (GLAST)………… These data suggest that GLAST may be involved in the regulation of neurotransmitter concentration in central nervous system.
o Storck, T, Schulte, S, Hofmann, K, & Stoffel, W. (1992). Structure, expression, and functional analysis of a na(+)-dependent glutamate/aspartate transporter from rat brain. Proceedings of the National Academy of Sciences (PNAS), 89(22), 10955-9.
Repeated intraventricular injection of the excitatory amino acids glutamate and aspartate for one hour produced morphologic changes in the hippocampus that were qualitatively identical to the acute and chronic changes seen in the brains of human epileptics and in experimental animals in which hippocampal seizure activity was induced by kainic acid or electrical stimulation of the perforant path. Light and electron microscopy revealed acute effects of glutamate and aspartate consisting of glial and dendritic swelling and neuronal soma necrosis ("dark cell degeneration"). Electron microscopy showed the focal dendritic swelling induced by glutamate or aspartate to be of the axon-sparing type with presynaptic terminals relatively unaffected. Four weeks after injection, irreversible neuron loss and reactive gliosis had occurred…….. Dendritic swelling induced by glutamate and aspartate in the cerebellar molecular layer was accompanied by acute necrosis of Purkinje cell somata. These results suggest that seizure-associated brain damage is initiated by excessive endogenous excitatory amino acid receptor activation.
o Sloviter, RS, & Dempster, DW. (1985). "epileptic" brain damage is replicated qualitatively in the rat hippocampus by central injection of glutamate or aspartate but not by gaba or acetylcholine. Brain Res Bull, 15(1), 39-60.