Can Echinococcus Granulosus Infestation Prevent Pancreatic Cancer? An invivo Experimental Study.

Hydatid cyst is a zoonotic infestation caused by Echinococcus granulosus, and it is known that some parasites found in humans cause cancer in humans or some may have a protective effect against cancer. Cancer is one of the most serious health problems of today and it has been shown in some studies that parasites such as Echinococcus granulosus can have an inhibitory effect. The aim of this study was determined as whether Echinococcus granulosus has an inhibitory effect on exocrine pancreatic cancer with the help of the azaserine-rat model used in different cancer studies.  Material and Methods: During experimental process a total of 45 male Wistar rats used, 14-day-old male Wistar rats were divided into groups according to the experimental protocol, administered azaserine injection protocol or kept as a control group without azaserine injection. Animals are grouped as Group 1, Control Group (group not treated with Azaserine and not injected with protoscolex.) (E-A-) (n=7); Group 2, Group injected with (IP) Azaserine only (30mg/kg) (E-A+)  (n=8);Group 3, Group injected (IP) with protoscolex suspension of 1 cc only (E+A-) (n=15);Group 4, Group injected both Azaserine (IP) and protoscolex suspension (IP) (E+A+) (n=15). Atypical Acinar Cell Foci (AACF) load in the exocrine pancreas of each rat was measured quantitatively with the help of a video image analyzer and the AACF load was calculated with the help of a mathematical model. Results: Findings showed that the Atypical Acinar Cell Foci (AACF) burden was statistically significantly lower in the Azaserine+ protoscolex (Azaserine-injected-protoscolex-implanted) rat group compared to the other groups, suggesting that Echinococcosis in the azaserine-rat model could inhibit the development of precursor foci of neoplastic changes in the exocrine pancreas. Conclusion: The most significant aspect of our study is that it contributes new insights into the controversy that Echinococcosis suppresses pancreatic cancer.

Effects of acetylsalicylic acid on rats: An in vivo experimental study in azaserine-rat model.

AIM: The effect of acetylsalicylic acid (ASA) on thiol levels was studied in a rat model of azaserine carcinogenesis. MATERIALS AND METHODS: ASA and azaserine were applied to the animals to research changes in cellular sulfhydryl (-SH) content and variations in free and protein-bound molecules containing the -SH group. Such effects in rats injected with azaserine were investigated at low (200 ppm) and high (400 ppm) concentrations of ASA over a relatively short (6 months) and a relatively long (12 months) period. RESULTS: Changes in the hepatic, pancreatic, and renal -SH contents were also determined. CONCLUSION: Compared to the other tissues studied, the liver contained the highest levels of both free and protein-bound -SH.

Potential neoplastic effects of parathion-methyl on rat liver.

The mutagenic and carcinogenic effects of parathion-methyl were examined by bacterial reverse mutation assay and a long-term experiment with wistar rats. The potential mutagenic effect of parathion-methyl in Salmonella typhimurium TA100 bacterial cells was observed without rat liver S9 metabolic activation. Parathion-methyl was further investigated for pathological changes in rat pancreas and liver. The long-term rat experiments showed that parathion-methyl exposure for 3 months can cause pathological changes in rat pancreases acinar cells and pancreatic hepatocytes. Atypical acinar cell focuses (AACF) were determined in the liver and pancreas of the rats. The results from short-term Ames test and long-term rat experiments suggested that parathion-methyl would be potential carcinogenic.

L-Cysteine influx and efflux: a possible role for red blood cells in regulation of redox status of the plasma.

The objective of this study was to investigate if erythrocytes play a role in the maintenance of redox homeostasis of the plasma. Thus, we studied L-cysteine efflux and influx in vitro in human erythrocytes. In the present study, we exposed the erythrocytes to different concentrations of L-cysteine and then measured the intracellular free -SH concentrations. Erythrocytes treated in the same manner were later utilized for the cysteine efflux studies. The effect of temperature on the influx and the efflux processes were also evaluated. Change in the free -SH content of the buffer was evaluated as a measure for the presence of an efflux process. The effects of free -SH depletion on L-cysteine transport is also investigated. We also determined the rate of L-cysteine efflux in the presence and absence of buthionine sulfoximine (BSO) in erythrocytes that are pretreated with 1-chloro-2,4-dinitro benzene, a glutathione (GSH) depletory. Our L-cysteine influx studies demonstrated that erythrocytes can respond to increases in L-cysteine concentration in the extracellular media and influx L-cysteine in a concentration-dependent manner. Free -SH concentrations in erythrocytes treated with 1 mM L-cysteine reached to 1.64 +/- 0.06 mM in 1 h whereas this concentration reached to 4.30 +/- 0.01 mM in 10 mM L-cysteine treated erythrocytes. The L-cysteine efflux is also determined to be time-and concentration-dependent. Erythrocytes that are pretreated with higher L-cysteine concentrations displayed a higher efflux process. Outside concentration of free -SH in 1 mM L-cysteine pretreated erythrocytes reached to 0.200 +/- 0.005 mM in 1 h whereas this concentration reached to 1.014 +/- 0.002 with 10 mM L-cysteine pretreated erythrocytes. Our results also indicate that the rate of inward and outward transport of L-cysteine is affected by the oxidative status of the erythrocytes. When GSH is depleted and GSH synthesis is blocked, the L-cysteine uptake and the efflux processes are significantly decreased. Depending on our results, it could be concluded that erythrocytes play a role in the regulation of the plasma redox status and intracellular level of GSH determines the rate of the L-cysteine efflux.

Methyl Parathion-Induced Changes in Free and Protein-Bound SH Levels in Rat Tissues.

The main objective of this study was to investigate the changes in free and protein-bound SH contents in methyl parathion-exposed rat tissues. The free and protein-bound SH levels are usually affected and depleted by oxidative stress-inducing agents. Results would indicate if methyl parathion toxicity partly results from depletion of sulfhydryl content of tissues. Six-week-old male Wistar albino rats were used in this study. Following exposure to methyl parathion for 3 months, the liver, the brain, and the kidney tissues were removed from the rats. The free and protein-bound SH contents were determined in these tissues. In addition, plasma lactate dehydrogenase levels were determined. Our results showed that methyl parathion exposure significantly lowers the free and protein-bound SH levels in rat tissues. However, lactate dehydrogenase activity in the blood plasma did not display any differences compared to the control group. The free SH concentrations in the control rat liver, brain, and kidney tissues were 3.78 +/- 0.1 mumol/100 mg tissue, 1.56 +/- 0.08 mumol/100 mg tissue, and 2.16 +/- 0.08 mumol/100 mg tissue, respectively, whereas the free SH concentrations in rats exposed to methyl parathion were determined as 0.536 +/- 0.1 mumol/100 mg tissue in the liver, 1.06 +/- 0.1 mumol/100 mg tissue in the brain, and 0.108 +/- 0.03 mumol/100 mg tissue in the kidney. The protein-bound SH concentrations in the liver and in the kidney in rats exposed to methyl parathion displayed a significant decrease also. However, the protein-bound SH level in the brain did not change significantly. These results indicate that methyl parathion exposure partially depletes the free and protein-bound SH levels. Thus, it was concluded that methyl parathion toxicity may partly result from oxidative stress.

Antisense oligonucleotides and prevention of tumor growth: a different approach and proposal for a new method.

There have been several attempts to prevent tumor formation and growth. However, none of the developed methods gives a completely satisfying result for the treatment of tumor masses. The most often used therapies against tumor cells are radiotherapy and chemotherapy. However, utilization of these methods to treat cancer generally result in generation of undesired side effects. In recent years, the antisense oligonucleotide technology has been employed, with success to an extent, in prevention of tumor growth. However, this method has its limitations. One of the most important limitation is that all of the crucial genes that play certain roles and are specifically expressed in tumor cells have not yet been identified. Therefore, only a few numbers of genes that are shown to play a role in tumor cells are targeted by the antisense oligonucleotide method. The aim of the present study is to propose a hypotheses and outline the involved procedure which could be used to generate oligonucleotides that are antisense to genes or mRNAs that display certain specific functions in tumor cells but are yet to be identified. The proposed hypotheses involves first, a careful isolation of differentially expressed mRNAs by using the tumor and the corresponding normal cells. These mRNAs should represent the genes that operate in tumor cells but not in the corresponding normal cells. Following the isolation of the differentially expressed mRNAs, they will be reverse transcribed and the desired amounts of cDNA copies will be obtained. The cDNA copies will then be used differentially as a source for oligonucleotides that are antisense to genes or mRNAs. To obtain the desired length oligonucleotides that will be used as antisense oligonucleotides the cDNA copies will be subjected to Maxam-Gilbert fragmentation and/or controlled enodonuclease digestion. These two mentioned procedures could be optimized and used together or separately to obtain the desired length oligonucleotides that will be used against tumor cells.