The effect of HLA-DP gene polymorphisms in Plasmodium Vivax-induced malaria susceptibility.

Plasmodium vivax is the second most common Plasmodium parasite causing clinically serious symptoms and death from malaria. It is an important cause of morbidity and mortality, especially in Asia, the Middle East, and South America. Human leukocyte antigen molecules are responsible for presenting foreign antigens to T cells. Polymorphisms in HLA genes affect antigen presentation. HLA alleles involved in the presentation of P. vivax antigens affect the antibody response. The present study aimed to reveal the relationship of rs3077 and rs9277535 polymorphisms in HLA-DP genes with malaria caused by P. vivax for the first time in the worldwide. In the present research, rs3077 and rs9277535 polymorphisms were investigated in a case-control study of 124 patients with P. vivax-induced malaria and 211 healthy persons by using a real-time polymerase chain reaction (RT-PCR). The results showed that the G alleles of rs3077 and rs9277535 polymorphisms were detected as protective alleles, while the A alleles of both polymorphisms increase the risk of susceptibility to malaria disease. The results of the present study showed that both polymorphisms have a major effect on the susceptibility to malaria caused by P. vivax. We recommend that this study should be conducted in a different population with a larger sample size to confirm our results.

The effect of Paraoxonase gene polymorphisms and paraoxonase enzyme activity on Non-Hodgkin lymphoma.

Non-Hodgkin Lymphoma (NHL) is a malignant lymphoproliferative disease. Antioxidant paraoxonase enzyme (PON1) has a vital role in the elimination of potential carcinogenic organophosphate molecules. The polymorphisms in the PON1 gene, especially Q192R and L55M, may affect negatively the activity and synthesis of PON1 enzyme. The aim of this study was to evaluate the effect of these polymorphisms together with PON1 enzyme activity on NHL. We surveyed these polymorphisms together with PON1 enzyme activity in 93 patients with NHL and in 93 healthy individuals by real-time polymerase chain reaction (RT-PCR) and spectrophotometer. Although carrying the M and R alleles of L55M and Q192R polymorphisms increases the risk of NHL, they were not significant. Furthermore, the NHL patients carrying 192 R allele had significantly lower enzyme activity than controls having same allele (P = 0.025). This research is the first study worldwide investigating the effect of Q192R and L55M polymorphisms on PON1 enzyme activity in NHL disease. The risk of developing NHL may be further increased in individuals with low enzyme activity having R risk allele of the Q192R polymorphism. The present study suggests that these polymorphisms in NHL disease should be analyzed together with PON1 enzyme activity in larger populations.Supplemental data for this article is available online at https://doi.org/10.1080/15257770.2022.2052315 .

Examination of the effect of curcumin in experimental liver damage created by diethylnitrosamine in Swiss albino mice to superoxide dismutase and catalase activities and glutathione, malondialdehyde, and advanced oxidation protein products levels.

In this study, the effects of curcumin, glutathione (GSH), malondialdehyde (MDA) levels, advanced protein oxidation products (AOPP), superoxide dismutase (SOD), and catalase (CAT) activities in experimental liver damage with diethylnitrosamine (DEN) in Swiss albino mice were investigated. The subjects (n = 9) used in the study were divided into 5 groups as tumor control 1, tumor control 2, curcumin protective, curcumin treatment and healthy control groups Curcumin oral gavage (in 150 mg/kg of ethylalcohol) was given to the protecting group for 19 days, 5 days before the administration of DEN, and 24 h after the administration of DEN. Hundred microliters of ethylalcohol oral gavage was given to the healthy group for 19 days. While MDA levels decreased significantly in the curcumin preservative group (p < 0.05), (p = 0.002), the decrease was not significant in the treatment groups (p > 0.05), (p = 0.128). AOPP levels decreased significantly in the curcumin protective group (p < 0.05), (p = 0.009) but the decrease in the treatment group was not found significant (p > 0.05), (p = 0.073). SOD activities increased significantly in both groups. It was found as (p < 0.05), (p = 0.001) and (p < 0.05), (p = 0.002), respectively. GSH levels decreased but these reductions were not found statistically significant. CAT activities increased significantly in both groups. It was determined as (p < 0.05), (p = 0.001) for both groups.

Association between chronic hepatitis B virus infection and HLA-DP gene polymorphisms in the Turkish population.

AIM: Hepatitis B virus (HBV) affects approximately 360 million people worldwide. 10-15% of patients with chronic HBV develop liver cirrhosis (LC), liver failure and hepatocellular carcinoma (HCC). Chronic HBV infection or HBV clearance is influenced by both viral and host factors. In genome-wide association studies (GWAS), the human leukocyte antigen (HLA) gene polymorphisms rs3077 and rs9277535 were identified to be associated with chronic hepatitis B. HLA genes have been linked to immune response to infectious agents. Genetic variants in HLA genes influence HLA mRNA expression which might also affect antigen presentation. We evaluated the association between HLA gene polymorphisms and the risk for persistent HBV infection. METHODS: In the current study, HLA gene polymorphisms were investigated in a case-control study of 294 chronic HBV patients and 234 persons with HBV natural clearance by using a real-time polymerase chain reaction (RT-PCR). RESULTS: The results showed that rs9277535 allele frequency is associated with HBV infection in the Turkish subjects examined (P=0.048). However, no association was found for rs3077. Additionally, the AG haplotype block showed a protective effect against the risk of persistent HBV infection (for the rs3077A/rs9277535G, OR=0.52; 95% 0.34-0.80, P=0.003). CONCLUSIONS: Our results, for the first time, demonstrate that HLA-DPB1 gene rs9277535A allele has a major effect on the risk of persistent HBV infection. We suggest that further independent studies are necessary to clarify the association of these polymorphisms with persistence or natural clearance of HBV infection in Caucasian populations.

Optimization of covalent immobilization of Trichoderma reesei cellulase onto modified ReliZyme HA403 and Sepabeads EC-EP supports for cellulose hydrolysis, in buffer and ionic liquids/buffer media.

The covalent immobilization of Trichoderma reesei cellulase onto modified ReliZyme HA403 and Sepabeads EC-EP supports were carried out. The optimal immobilization conditions were determined using response surface methodology. The hydrolysis of cellulose using the free and immobilized cellulase preparations in ionic liquids (IL) using cosolvents was investigated. The hydrolytic activities in buffer medium containing 25% (v/v) of 1-butyl-3-methylimidazolium hexafluorophosphate were around 2.6-, 1.6-, and 5.5-fold higher than the activities in buffer medium. The retained initial activities were 32% and 57%, respectively for cellulase preparations immobilized onto Sepabeads EC-EP support and onto modified ReliZyme HA403 support after 5 reuses.

Modulating actions of NMDA receptors on pronociceptive effects of locally injected remifentanil in diabetic rats.

BACKGROUND: In this study, we investigated the effects of locally (intraplantar) applied remifentanil, a µ opioid receptor agonist, to the paws and tested whether locally N-methyl d-aspartate (NMDA) receptors agonist or antagonist can modify remifentanil-induced effects in diabetic rats. METHODS: Effects of locally (intraplantar) remifentanil, NMDA and MK801 or their combinations were investigated by measuring the latencies, thresholds and two biochemical parameters (malondialdehyde (MDA) and nitric oxide (NO)), in streptozotocin induced diabetic rats. RESULTS: Diabetic rats exhibited hyperalgesia and allodynia and remifentanil treatment aggravated the hyperalgesia and allodynia. The hyperalgesic and allodynic effects of remifentanil decreased in diabetic rats as compared to healthy rats. MK801 suppressed the hyperalgesic and allodynic actions of remifentanil in diabetic rats. However, hyperalgesic and allodynic actions of NMDA increased in diabetic rats. In contrast to age matched group, the combination of NMDA and remifentanil did not produce synergistic actions in diabetic rats. The levels of MDA and NO in the paw tissues of the diabetic rats significantly increased. MK801 significantly decreased NO levels, but not MDA, in diabetic rats. CONCLUSIONS: The hyperalgesic and allodynic actions of locally treated remifentanil may decrease in diabetic conditions. Increases in NMDA receptors activation, reactive oxygen species production and NO release may modify the sensitivity to remifentanil in diabetes induced neuropathic pain states.

Oxidative stress in vivax malaria.

Malaria is still a leading cause of morbidity and mortality. The increase in lipid peroxidation reported in malaria infection and antioxidant status may be a useful marker of oxidative stress during malaria infection. The aim of this study was to investigate the role of antioxidant enzymes against toxic reactive oxygen species in patients infected with Plasmodium vivax and healthy controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were determined in 91 P. vivax patients and compared with 52 controls. Malondialdehyde levels, superoxide dismutase, and glutathione peroxidase activities were 8.07±2.29 nM/ml, 2.69±0.33 U/ml, and 49.6±3.2 U/g Hb in the patient group and 2.72±0.50 nM/ml, 3.71±0.47 U/ml, and 62.3±4.3 U/g Hb in the control group, respectively. Malondialdehyde levels were found statistically significant in patients with vivax malaria higher than in healthy controls (P<0.001). On the other hand, superoxide dismutase and glutathione peroxidase activities were found to be significantly lower in vivax malaria patients than in controls (P<0.05). There was an increase in oxidative stress in vivax malaria. The results suggested that antioxidant defense mechanisms may play an important role in the pathogenesis of P. vivax.

Serum malondialdehyde level in patients with cystic echinococcosis.

OBJECTIVE: To investigate the changes of serum malondialdehyde (MDA) level for the oxidative stress hypothesis in patients with cystic echinococcosis (CE). METHODS: The study was conducted on patients with CE before the surgical treatment. Anti-Echinococcus granulosus antibodies were determined by serological method. We assayed MDA activities measured of 57 subjects and matched in 45 healthy controls. This study took place in the Faculty of Medicine, University of Cukurova, Balcali Hospital in Adana, Turkey, between March 2004 and October 2005. RESULTS: The mean +/- SD of MDA levels of patients with CE was 6.70 +/- 1.66 and healthy controls was 2.53 +/- 0.43. The difference between MDA levels of patients and controls was statistically significant (p<0.001). CONCLUSION: The high infection/control ratio of MDA concentration and the significant correlation strongly indicate the occurrence of oxidative stress and lipid peroxidation as a mechanism of tissue damage in cases of CE. Our study highlights the usefulness of serum markers to investigate complex pathological situations, including distinct forms of chronic liver inflammation associated with CE.

Free radicals and antioxidants in primary fibromyalgia: an oxidative stress disorder?

The role of free radicals in fibromyalgia is controversial. In this study, 85 female patients with primary fibromyalgia and 80 age-, height-, and weight-matched healthy women were evaluated for oxidant/antioxidant balance. Malondialdehyde is a toxic metabolite of lipid peroxidation used as a marker of free radical damage. Superoxide dismutase is an intracellular antioxidant enzyme and shows antioxidant capacity. Pain was assessed by visual analog scale. Tender points were assessed by palpation. Age, smoking, body mass index (BMI), and duration of disease were also recorded. Malondialdehyde levels were significantly higher and superoxide dismutase levels significantly lower in fibromyalgic patients than controls. Age, BMI, smoking, and duration of disease did not affect these parameters. We found no correlation between pain and number of tender points. In conclusion, oxidant/antioxidant balances were changed in fibromyalgia. Increased free radical levels may be responsible for the development of fibromyalgia. These findings may support the hypothesis of fibromyalgia as an oxidative disorder.

The effects of the caffeic acid phenethyl ester (CAPE) on erythrocyte membrane damage after hind limb ischaemia-reperfusion.

Reactive oxygen species have been implicated in pathogenesis injury after ischaemia-reperfusion (I/R). Caffeic Acid Phenethyl Ester (CAPE), an active component of honeybee propolis extract, exhibits antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects of CAPE on erythrocyte membrane damage after hind limb I/R. Rats were divided into two groups: I/R and I/R with CAPE pre-treatment. They were anaesthetized with intramuscular ketamine 100 mg kg(-1). A 4-h I/R period was performed on the right hind limb of all animals. In the CAPE-treated group, animals received CAPE 10 microm by intraperitoneal injection 1 h before the reperfusion. At the end of the reperfusion period, a midsternotomy was performed. A 5-ml blood sample was withdrawn from the ascending aorta for biochemical assays. Serum and erythrocyte membrane MDA levels were significantly lower in the CAPE-treated group when compared to the I/R group ( p = 0.001 and p<0.001, respectively). Erythrocyte membrane Na(+)-K(+) ATPases activity in the CAPE-treated group was significantly higher than the I/R group ( p<0.001). In conclusion, CAPE seems to be effective in protecting against oxidative stress. Therefore, we suggest that in order to decrease I/R injury, pre-administration of CAPE may be a promising agent for a variety of conditions associated with I/R.

Effects of lead on Na(+)-K(+) ATPase and Ca(+2) ATPase activities and lipid peroxidation in blood of workers.

Lead is considered one of the major environmental toxicants that causes hematological, neurological, and gastrointestinal dysfunction. In this study, the authors examined the relationship between lead and lipid peroxidation, lead and Na(+)-K(+) ATPase activity, and lead and Ca(+2) ATPase activity in blood of workers. The working group consisted of 30 male workers occupationally exposed to lead at least for 10 years. The control group consisted of 20 healthy male individuals not involved with job-related lead exposures. Blood lead content of the control group and the working group were 10.0 +/- 1.8 microg/dl and 317.3 +/- 47.6 microg/dl, respectively. Malondialdehyde (MDA) value of the working group (0.57 +/- 0.30 nmol MDA/ml) was significantly greater than MDA value of the control goup (0.17 +/- 0.02 nmol MDA/ml). In the working group, both Na(+)-K(+) ATPase activity (105.0 +/- 47.0 nmol Pi. mg protein(-1) x h(-1)) and Ca(+2) ATPase activity (58.0 +/- 40.0 nmol Pi. mg protein(-1) x h(-1)) were lower compared with the corresponding values of Na(+)-K(+) ATPase activity (247.0 +/- 41.0 nmol Pi. mg protein(-1) x h(-1)) and Ca(+2) ATPase activity (230.0 +/- 41.0 nmol Pi. mg protein(-1) x h(-1)) of normal controls. The results show that lead exposure causes inhibition of Na(+)-K(+) ATPase and Ca(+2) ATPase activities and also results in increased lipid peroxidation.