Implication of High-mobility group box-1 and skin post mortem changes in estimation of time passed since death: Animal and human study.

Determination of postmortem interval (PMI) is one of the goals of the forensic autopsy. The study aimed to correlate the postmortem skin changes and High-mobility group box-1 (HMGB1) alterations in serum and skin immunohistochemical staining with time since death. We used animal and human specimens; forty adult male albino rats were dissected to obtain samples at PMI (0, 3, 6, 12, 24 h); forty human medicolegal autopsy cases with a known time of death (within the first 24 h PMI). Cases were classified into 5 groups according to the PMI: I (0 h); II (≤3h); III (4 to 6); IV (7 to 12); V (13 to 24) hour intervals after death; blood and full-thickness skin samples were collected from both models. Results showed a significant time-dependent elevation in serum HMGB1 levels along with its overexpression in immunohistochemically stained skin tissue. Also, the degree of histopathological changes in epidermis, dermis, and hypodermis progressively increased with PMI in both models. The timetable of postmortem skin histological changes, serum HMGB1 concentration, and immunoexpression for HMGB1 proteins in skin tissues has a profile that could serve as actual and simply convenient parameters for accurate determination of postmortem intervals in both models. HMGB1 displayed a pivotal role in the estimation of PMI at the examined periods.

Impact of e-cigarettes on colonic mucosa and the role of recovery: involvement of oxidative and inflammatory pathway.

Electronic cigarettes (e-cigarettes) (EC) are often advertised as a safer alternative to conventional cigarettes. Its widespread use has led to increased interest in its adverse health effects, thanks to few restrictions and a lack of regulatory guidelines. The study aimed to evaluate the influence of exposure to e-cigarette aerosol inhalation in rat colon model and conduct a follow-up after cessation of exposure. The experiment included 30 male adult Albino rats. The animals were divided into three groups: group I (control), non-exposed animals; group II (exposed), was exposed to electronic cigarette liquid vapor for four consecutive weeks; and group III (recovery), was followed up for another 4 weeks after exposure to an e-cigarette as exposed group and for the same duration. In the exposed group, malondialdehyde (MDA) and total nitric oxide (NO) increased significantly in colonic tissue, while superoxide dismutase (SOD) decreased. On histological examination, colonic mucosa showed distortion and loss of its epithelial lining with heavy inflammatory cell infiltration. Also, there was a significant decrease in periodic acid-Schiff-positive goblet cells and area percent of proliferating cell nuclear antigen expression. Tumor necrosis factor-alpha (TNFα) expression significantly increased in colonic mucosa. After 4 weeks of EC cessation, the colonic mucosal histological structure showed recovery with downregulated TNFα immunoexpression and restored oxidant/antioxidant balance. In conclusion, the usage of electronic cigarettes resulted in marked pathological alterations in the colonic mucosa, which could be attributed to oxidative and inflammatory stresses. In contrast, the cessation of exposure led to recovery.

Modulatory effects of catechin hydrate on benzo[a]pyrene-induced nephrotoxicity in adult male albino rats.

Benzo [a] pyrene (B[a]P) is a potent mutagen and carcinogen, considered one of the commonest concomitants in the environment. The study aimed to evaluate the effect of catechin hydrate on benzo pyrene-induced kidney toxicity. Thirty-six adult male albino rats were divided into six groups: group I untreated control, group II received 10 mL/kg of corn oil (solvent of benzo [a] pyrene) twice a week, group III received 1 mL/kg 0.5% dimethyl sulfoxide (DMSO) (solvent of catechin) once per day, group IV received 50 mg/kg body weight of benzo[a]pyrene twice a week, group V received 20 mg/kg body weight of catechin in 1 mL/kg 0.5% DMSO once daily, and group VI received both catechin+benzo [a] pyrene with the same doses. All treatment was given by oral gavage for four weeks. At the end of the experiment, blood samples were collected for biochemical investigations, tissues were obtained for genotoxicity, RT-PCR, and histopathological studies. B[a]P exposure induced an increase in serum urea and creatinine levels along with severe renal histopathological changes. Our results showed a subsequent decrease in the antioxidant enzyme activities (catalase and superoxide dismutase), and conversely, (malondialdehyde) levels markedly elevated. Also, B[a]P induced DNA damage as well as activated an apoptotic pathway confirmed by upregulation of Bax, caspase-3, and downregulation of Bcl-2 expression. However, treatment with catechin-corrected kidney functions and antioxidant enzymes as well as regulated apoptosis. Histological results also supported the protective effects of catechin. These findings suggested that catechin hydrate is an effective natural product that attenuates benzo pyrene-induced kidney toxicity.

Effects of catechin hydrate in benzo[a]pyrene-induced lung toxicity: roles of oxidative stress, apoptosis, and DNA damage.

The major sources for human exposure to Benzo [a] pyrene (B[a]P) are contaminated food, water, and inhalation of polycyclic aromatic hydrocarbon. B[a]P is a well-known human genotoxic carcinogen (IARC Group 1). It has a tumorigenic potential in virtually all in vivo experimental animal model systems. The study aimed to evaluate the effect of catechin hydrate (CH) against B [a] P-induced toxicity in the lung of adult albino rats. Thirty-six adult male albino rats (150-200 g) were divided into six groups, three control groups, and three experimental groups: B[a] P-treated group, (CH)-treated group, and B[a] P+(CH)-treated group. At the end of the fourth week of the study, blood samples and lung tissues were obtained for the biochemical and genotoxicity, RT-PCR, histopathological, and immunohistochemical investigations, respectively. Our results clarified that B[a] P exposure caused a subsequent decrease in the activities of antioxidant enzymes (SOD, CAT), and conversely (MDA) levels elevated markedly. Also, B[a] P induced DNA damages and activated the apoptotic pathway, presented by upregulated Bax, caspase-3, and downregulated Bcl-2 gens. However, treatment with CH increased antioxidant enzymes as well as regulated apoptosis. Discernible histological changes in the lung also supported the protective effects of CH. These findings suggested that CH is an effective natural product that attenuates Benzo [a] pyrene-induced lung toxicity.