Liver cell membrane antibody, kidney injury molecule and lungs tumour antigen expression on the MCF-7 cell induced breast cancer administered with Citrus limon juice and tamoxifen in Sprawgue dawley rats

Monitoring and evaluation have been one of the major measures to determine possible progression of response of disorder to the alternative treatments, however Anti-Liver Cell membrane Antibody, Kidney Injury Molecule and Lungs Tumour Antigen Expression on the MCF-7 Cell Induced Breast Cancer Rats administered with Citrus Limon juice and Tamoxifen were carried out, Over one hundred and twenty Sprague dawley rats of 40 days old average body weight 180-220g were divided into ten (10) containing of 12 animals per group, group 1 was control, fed only with rat chow and water, group 2 was MCF-7 cell line induced rats alone (BCIR only), group 3 Citrus Limon juice (CLJ) at 8.88%, Group 4 Citrus Limon juice (CLJ) at 17.32%, group 5 Citrus Limon juice (CLJ) at 25.98%, group 6 was given 0.2mg/kg of Tamoxifen alone, group 7 (BCIR+CLJ at 8.88%), group 8 (BCIR+CLJ at 17.32%), group 9 (BCIR+CLJ at 25.98%) and group (BCIR+ 0.2mg/kg of Tamoxifen). Acute and sub – acute toxicity were carried out after the establishment of safety dose following determination of LD50, on the fresh Citrus Limon juice Breast cancer induction and Tumor sizes were analysed. At the end of the administration, animals were sacrificed, fresh blood was taken, centrifuged at 3000 rpm, serum was collected and stored at 8oc Breast Cancer Tumor Associated Assays, Kidney Injury, Liver cell Membrane Antibody and Lung Tumor Antigens were analysed. Result, Mammary tumor induction was succeeded in all the MCF-7 cell line induced groups with minimum number of morbidity. Tumor size was significantly increase in tumor mass BCIR only at P>0.001 when compared to BCIR + CLJ and BCIR + Tamoxifen groups. Immunoogical expression of Breast Cancer Associated Tumor revealed significant increase suppressor gene/protein, Immunocytochemical in-vivo of Breast Cancer Associated Organs showed significant increase in KIM , LCMA and LTA at P>0.001 in BCIR when compared to all the BCIR + CLJ, BCIR + Tamoxifen and other non-BCIR groups. In conclusion, this study showed that KIM , LCMA and LTA exhibited strong Immunochemical expression of Citrus Limon juice potency possessing possible anticancer activities without posing pathological conditions on the body during and after usage, hence KIM, LCMA and LTA are demonstrated to be valuable in the monitoring and evaluation progression of tumor as Citrus Limon Juice could be used as alternative therapy in the treatment of Breast cancer that are hormonal dependant in similar manner to Tamoxifen.

Physiological effect of circulating glucagon on the hepatic membrane potential

The pancreatic hormone glucagon hyperpolarizes the liver cell membrane under various conditions. Here we investigated the physiological relevance of this effect by testing the influence of infusions of glucagon antiserum on the liver cell membrane potential in vivo. Intracellular microelectrode recordings of liver cells (up to 60/rat over 2 h) were done in anesthetized male rats. Livers were fixed in place, and recordings were done 10–30 min after intraperitoneal injections of glucagon or hepatic portal vein infusions of glucagon or specific polyclonal glucagon antibodies raised in rabbits. The isotonic lactose vehicle was used as a control for glucagon, and equal amounts of nonimmunized rabbit IgG were used as a control for glucagon antibodies. Intraperitoneal glucagon (400 μg/kg) hyperpolarized the liver cell membrane up to 12 mV, and intraportal glucagon (10 or 60 μg/kg) dose dependently hyperpolarized the liver cell membrane by 3–7 mV. Intraportal infusion of glucagon antiserum (in vitro binding capacity of 4 ng glucagon/rat) significantly depolarized the liver cell membrane by ∼2.5 mV. The effects of both glucagon and glucagon antiserum reversed after 60–90 min. We conclude that glucagon is a physiologically important modulator of the liver cell membrane potential.

Hyperpolarization of hepatocytes by 2,5-AM: implications for hepatic control of food intake

Because 2,5-anhydro-D-mannitol (2,5-AM) seems to stimulate feeding by acting on the liver and because the hepatic membrane potential has been suggested to play an important role in control of feeding ("potentiostatic" hypothesis), we investigated the effect of 2,5-AM on the membrane potential of liver cells with microelectrodes using a superfused liver slice technique. 2,5-AM (2.5 mM), which reduces intracellular ATP in rat liver, hyperpolarized the liver cell membrane in mouse and rat liver slices by 4-7 mV. This hyperpolarization was reversed by quinine (1 mM), an unspecific blocker of Ca2+-dependent K+ channels, and abolished by apamin (20 nM), a blocker of Ca2+-activated K+ channels with low conductance. Amiloride at 10(-3) M, but not at 10(-6) M, or a low-Na medium (26 mM) also eliminated the hyperpolarization. The K+ channel blockers cetiedil (50 microM), glibenclamide (30 microM), and Ba2+ (5 mM); flufenamic acid (100 microM), a blocker of nonselective cation channels; and ouabain (1 mM), an inhibitor of the Na+-K+-adenosinetriphosphatase, did not significantly influence the 2,5-AM-induced hyperpolarization. It is concluded that 2,5-AM hyperpolarizes the liver cell membrane by activating Ca2+-dependent K+ channels. This activation seems to be impaired when the Na+/H+ exchanger is inhibited by amiloride or a low-Na+ medium. The findings also imply that the hyperphagic effect of 2,5-AM observed in rats is not associated with a decrease in the hepatic membrane potential, as postulated by the potentiostatic hypothesis.