Among the Iranian freshwater fishes, Luciobarbus esocinus, L. xanthopterus, Mesopothamichthies sharpeyi, and Tor grypus have a good growth rate in nature bringing its proposals on their controlled breeding and cultivation. This study aimed to analyze the mitochondrial phylogeny of L. esocinus, L. xanthopterus, M. sharpeyi, and T. grypus. In this study, the sequences of Cytochrom Oxidase subunit one (COI) was used. The specimens analyzed here were collected from Shadegan Wetland (Khuzistan Province, Iran) and rivers of the Tigris basin in Ghasr-e-Shirin, Iran. Based on the results, it is shown that T. grypus and M. sharpeyi are phylogenetically closely related and closely affined to the genus Tor. In addition, it is shown that L. esocinus and L. xanthopterus are closely related (0. 6% K2P distance), which may indicate a recent divergence of them or possible hybrid origin for one of them. Finally it can be inferred that M. sharpeyi and T. grypus are affined to the Oriental (East Asian) and Indian species, but have diverged in the Mesopotamia and L. esocinus and L. xanthopterus are not affined to the Asian species but have Palearctic origin.

Many studies have shown that viruses after they enter the host cell can interact with mitochondria and disrupt their function; particularly some studies have determined that these effects can alter the mitochondrial structure as well as changes in the pathway for energy production. The effect of virus or viral protein on the electron transport chain, sometimes following entry of divert viruses to the host cell, will result in a sharp decrease in cellular energy at the end of the electron transport process. In addition, nowadays new data indicate that a number of viruses may affect the mitochondrial pathway of apoptosis and thus affect the respiratory chain in the mitochondria. Such effects can lead to clinical outcomes, particularly in the context of sustained infections, which can ultimately be considered as a possible cause of chronic fatigue syndrome (CFS). Therefore, as a hypothesis, it may be concluded that viral infections may be one of the main potential etiology for this syndrome.

Background: Methamphetamine (METH) is considered the second most commonly abused drug in the world. There is limited or no evidence concerning the effective treatment of METH withdrawal symptoms, such as depression and anxiety. Mode of action of selegiline (increase of the brain neurotransmitter activity) suggests that it might be useful in METH withdrawal syndrome treatment, being capable of diminishing the preference and depression involved in drug degeneration and addictive activities. Methods: Mice were randomly divided into 10 groups (n= 10): five METH-nondependent groups treated with normal saline intraperitoneal (i. p) for two weeks, to which, from the 15th day, selegiline (10, 20 and 40 mg/kg; i. p) or fluoxetine (5 mg/kg; i. p) was administrated for 10 consecutive days. Other groups injected METH (2 mg/kg, at 12-h intervals) for 14 days. From the 15th day, the 10-day period of METH abstinence started and the above-mentioned doses of selegiline or fluoxetine were injected. Then, the mice were evaluated for depression and biochemical assessments from the 25th day of the study. Results: The data indicated that post-treatment with selegiline (10-40 mg/kg; i. p) for 10 days reversed METH-induced depressive-like behaviors in the forced swimming test (FST), tail suspension test (TST), and splash test with exerting no effects on the locomotor activity. Furthermore, none of the previously proposed treatments affected the behavioral abnormality in the control animals. Moreover, both selegiline and fluoxetine as standard antidepressant drug, substantially improved the levels of mitochondrial reduced glutathione (GSH), malondialdehyde (MDA), and adenosine triphosphate (ATP). Conclusion: Our findings demonstrated that selegiline produced antidepressant-like effects following METH withdrawal and prevented the mitochondrial dysfunction in the male mice.

Background & Objectives: Formation of myelin depends on maturation and development of the axonal cytoskeleton andmitochondria. Collagen gel can specifically play role in the regulation and development of axonal cytoskeleton.Methods: This research is an experimental study in which forty eight male rats (200-250g) were used. After axotomy, 1 cm segment of the sciatic nerve in rats was removed, and the gap was then bridged by one of the four following methods: polyvinylidene fluoride or PVDF + Collagen gel, Autograft, sham and control. Sciatic nerve was studied by electron microscope by the end of the 4th week and the 12th week.Results: By the end of the 4th week after the regeneration the number of unmyelinated axons in autograft and Collagen Gel was not significant, by the end of the 12th week, the number of unmyelinated axons in autograft group was superior to that of nerve growth factor group (P<0.01). After 12 weeks of regeneration, microtubular density values of normal and autograft groups were not statistically different. The cristae of axonal mitochondria in experimental groups are orientate parallel with its long dimension.Conclusion: The results of study indicated that because of its positive effect on the growth and development of microtubules and mitochodria, collagen Gel combination with PVDF can be used to repair peripheral nerve injuries.

Objective(s): Diabetes is fundamentally connected with the inability of skeletal muscle. Sinapic acid (SA) has multiple biologic functions and is diffusely utilized in diabetic complications. The purpose of this study was to explore the potential improvement effect and mechanisms of SA in streptozotocin (STZ)-induced diabetic muscle atrophy. Materials and Methods: The model of diabetic mice was established by intraperitoneal STZ (200 mg/kg) to evaluate the treatment effect of SA (40 mg/kg/d for 8 weeks) on muscle atrophy. Muscle fiber size was assessed by Hematoxylin and Eosin (HE) staining. Muscle force was measured by a dynamometer. Biochemical parameters were tested by using corresponding commercial kits. The expressions of Atrogin-1, MuRF-1, nuclear respiratory factor 1 (NRF-1), peroxisome proliferative activated receptor gamma coactivator 1 alpha (PGC-1α ), CHOP, GRP-78, BAX, and BCL-2 were detected by Western blot. Results: Our data demonstrated that SA increased fiber size and weight of gastrocnemius, and enhanced grip strength to alleviate diabetes-induced muscle atrophy. In serum, SA restrained creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), tumor necrosis factor (TNF-a), and interleukin 6 (IL-6) levels, while enhancing total anti-oxidant capacity (T-AOC), superoxide dismutase (SOD) and catalase (CAT) levels to improve muscle injury. In gastrocnemius, SA promoted NRF-1, PGC-1α , and BCL-2 expressions, while inhibiting Atrogin-1, MuRF-1, CHOP, GRP-87, and BAX expressions. Conclusion: SA protected against diabetes-induced gastrocnemius injury via improvement of mitochondrial function, endoplasmic reticulum (ER) stress, and apoptosis, and could be developed to prevent and treat diabetic muscle atrophy.

Wild boars may be infected with several zoonotic parasitic infections including Fasciola spp. We reported a case of Fasciola infection in a wild boar in Bushehr Province in southwestern Iran. The sample was isolated from the liver of a hunted wild boar. A few of adult worms were fixed and stained. DNA was extracted from apical and lateral parts of the worms and PCR amplified, targeting NADH dehydrogenase subunit 1 (nad1) and cytochrome C oxidase subunit 1 (cox1) MITOCHONDRION genes. Although the worm was quite long and looked much similar to F. gigantica, sequencing and analysis of PCR products of nad1 and cox1 genes revealed that the isolate has the most similarity with F. hepatica. This is the first report of molecular evaluation of Fasciola spp. from wild boar in Iran.

Letter to the Editor With interest, we read the review article by Ahmadabadi et al. on autism spectrum disorders (ASDs) in inborn errors of metabolism (IEM) (1). They reviewed 37 studies, and found that IEMs underlie autistic features in <5% of the patients, and that there is growing evidence on the association between ASDs and mitochondrial disorders (MIDs), including mitochondrial encephalopathy, lactic acidosis, stroke-like episodes (MELAS) syndrome, and respiratory chain complex III/IV deficiency (1). The authors concluded that the syndromic autism, a strong family history, or consanguinity suggest IEM (1). However, we have raised the following comments and concerns: We disagree with the idea that mitochondrial disorders (MIDs) have only two points of onset as they can occur at any age, and their broad variability, even in a family, results from the peculiarities of mitochondrial genetics. Due to mutations in mtDNA-located genes, MIDs are maternally transmitted, and the underlying mtDNA mutations may not occur in each mtDNA copy (heteroplasmy). Moreover, mtDNA copy number may considerably vary from one MITOCHONDRION to another MITOCHONDRION, particularly if the mutation is located in a nuclearly-encoded gene. MIDs frequently manifest in the central nervous system (CNS), and the CNS manifestations may include psychiatric or neurological diseases or both. The psychiatric diseases range from mild cognitive impairment and personality change to delirium and psychosis. Autism has been frequently reported in MIDs (2) and may or may not be associated with cerebral morphological alterations. We also disagree that ASD occurs only in MELAS and complex-III/ IV deficiency (1). ASD has also been reported in a patient carrying the mtDNA variant m. 8363G>A, whose sister was carrying the same variant and presented with Leigh syndrome (3), as well as in two Korean siblings carrying the variant c. 790C>T in TFB2M (4). In a study on 60 ASD patients, single mtDNA deletions were detected in 16. 6% of the patients (5). In the same study, the ten patients with mtDNA deletions also carried single nucleotide variants (SNVs) in ASD-associated genes (5). In a study on 95 ASD patients, the mtDNA content decreased in the ASD patients, and 49 putative pathogenic mtDNA variants were detected (6). In a study on 10 families with ASD, whole-exome sequencing revealed the variants of interest (VOIs) in the ND5 gene in one family and VOIs in ATP6 and NDUFS4 in another family (7). In a study on 24 Iranian ASD patients, mtDNA mutations 16126T>C, m. 14569G>A, and m., 1811A>G, all of which were located in non-coding regions, showed a significant relationship with ASD (8). In general, there is ample evidence indicating that the IEM, which is most frequently associated with ASD, is MID. According to the literature, the mtDNA variants but not the nDNA variants have been more frequently associated with ASD. Patients with an ASD should be first examined in terms of the presence or absence of MID.

Leishmania infantum is the causative agent of infantile visceral leishmaniasis (VL) in the Mediterranean region. Despite developing protective responses, the disease progresses due to many of factors. These include the action of suppressive cytokines, exhaustion of specific T cells, loss of lymphoid tissue, and defective humoral response. Genetic changes that occur inside the genome of alienated or parasite cells, along with immune responses, play an important role in controlling or progressing the disease. Proapoptotic proteins such as Smac/DIABLO, EndoG, AIF (apoptosis‑ inducing factor), and cytochrome C are effective in apoptosis. EndoG is a MITOCHONDRION‑ specific nuclease that translocates to the nucleus during apoptosis. Once released from mitochondria, endoG cleaves chromatin DNA into nucleosomal fragments independently of caspases. Therefore, endoG represents a caspase‑ independent apoptotic pathway initiated from the mitochondria. A comprehensive understanding of the immune and genetic events that occur during VL is very important for designing immunotherapy strategies and developing effective vaccines for disease prevention. In this review which explained the immunological responses and also the important factors that can contribute to parasite apoptosis and are used in subsequent studies as a target for the preparation of drugs or recombinant vaccines against parasites are briefly reviewed.