Oxaliplatin is a water-soluble platinum complex. It has a cytotoxic effect on tumor cells. Its antitumor activity will not be influenced by the DNA mismatch repair defects or enhancement of replication.
It has no cross resistance with bypass cisplatin or carboplatin. It also has a synergistic effect with other anticancer drugs, especially the collaborative application of 5-FU can be maintained in5-fluorouracil-resistant cell lines. It is mainly used in clinical treatment of advanced colorectal cancer, gastric cancer, breast cancer, ovarian cancer, and so on. The common adverse reaction is peripheral sensory neurotoxicity involving in the sensory nerve endings, thus limiting the further influence of drug dose and clinical efficacy.
Oxaliplatin is a third generation platinum anticancer drug after cisplatin and carboplatin for pharmaceutical raw materials suppliers. The outer peripheral neuropathy is the major dose-limiting toxicity. The clinical symptoms can be divided into two categories: acute neurotoxicity, the rapid onset of the cold-sensitive peripheral nerve paresthesia or sensory impairments, such as fingers and toes end of numbness or sensory loss, insensitivity of oral and throat, and occasionally muscle rigidity, laryngeal spasm, difficulty breathing, and aphasia. Speed hair paresthesia of the more common, these symptoms more than a few days disappeared. The accumulation of late-onset sensorineural disorders, multiple cycle medication dose due to cumulative toxicity, peripheral neuropathy, showing the lack of depth of feeling, sensory ataxia and weakened. The toxicity was dose-dependent, cumulative dose is more, sensory disturbances will be the longer duration. The accumulation of delayed feeling of neurological disorders generally will gradually recover after stopping. Generally, the median recovery period is 15 weeks.
Oxaliplatin neurotoxicity mechanism is not clear that the main mechanism has two aspects, one platinum itself accumulation caused; the other hand, that by its metabolite oxalic acid (salt) cause. Platinum drug-induced neurotoxicity is caused by the accumulation of platinum peripheral nervous system, the main site of injury may be the dorsal root neurons in the spinal cord; platinum accumulation level in the nervous system, from largest to smallest order of the dorsal root central nervous the nerve root, peripheral nerve. Other symptoms of neurotoxicity of research table Mingaoshali platinum, also from the special role of ion channels in the cell membrane and found that oxaliplatin led to a mixture of action potential amplitude and duration increase, thereby prolonging the refractory period of peripheral nerve, prompted it to affect the voltage-controlled sodium ion channels.
Further studies revealed that this sodium channel change is caused by oxaliplatin in vivo metabolite oxalate. Glutathione drugs can prevent the platinum compounds, the initial accumulation of spinal dorsal root central neurons, the same time, it can be combination of thiol free radicals, can be converted into easy to metabolic acids in order to accelerate the excretion of free radicals, help alleviate chemotherapy side effects, no significant impact on the efficacy of chemotherapy; synthesis. It can protect the liver detoxification function.
Ca2 + can change the characteristics of voltage-dependent sodium channels, increase intracellular calcium concentration, affect the hyperpolarization of the cell membrane and promote the effect of closure of the sodium channel. Mg2 + has impact on the biofilm from the multifaceted way with a strong membrane stabilizing characteristics. It is an active agent for plasma membrane Na +-K +-ATPase and it is conducive to the functioning of the sodium pump. Cholinesterase, choline acetyltransferase relating to the transmission of nerve impulses can not live without the presence of Mg2 +. So in nerve impulse transmission and the maintenance of neuromuscular stress, magnesium plays an important role. Therefore, the incidence and severity of oxaliplatin-induced peripheral neurotoxicity are significantly decreased by using the mixture agents of glutathione, calcium and magnesium.Source:http://www.cospcn.com
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