Global burden of prostate cancer attributable to smoking among males in 204 countries and territories, 1990-2019.

INTRODUCTION: Understanding the latest global spatio-temporal pattern of prostate cancer burden attributable to smoking can help guide effective global health policy. This study aims to elucidate the trends in smoking-related prostate cancer from 1990 to 2019 using Global Burden of Disease (GBD) 2019 study data. METHODS: Data on prostate cancer attributable to smoking were extracted from Global Burden of Disease Study (GBD) 2019. The numbers and age-standardized rates on smoking-related prostate cancer mortality (ASMR) and disability-adjusted life years (ASDR) were analyzed by year, age, region, country, and socio-demographic index (SDI) level. Estimated annual percentage change (EAPC) was calculated to evaluate the temporal trends of ASMR and ASDR from 1990 to 2019. RESULTS: Of all prostate cancer deaths and DALYs globally in 2019, 6% and 6.6% were attributable to smoking, which contributed to 29,298 (95% CI 12,789 to 46,609) deaths and 571,590 (95% CI 253,490 to 917,820) disability-adjusted life-years (DALYs) in 2019. The number of smoking-related deaths and DALYs showed an upward trend, increasing by half from 1990 to 2019, while ASMR and ASDR declined in five sociodemographic indexes (SDI) regions, with the fastest decline in high SDI regions. For geographical regions, Western Europe and East Asia were the high-risk areas of prostate cancer deaths and DALYs attributable to smoking, among which China and the United States were the countries with the heaviest burden. The ASMR has decreased in all age groups, with the fastest decrease occurring in 75-79 years old. The ASMR or ASDR tended to increase in countries with the lowest SDI, but declined in countries with the highest SDI. The EAPC in ASMR or ASDR was highly negatively correlated with Human Development Index (HDI) in 2019, with coefficients 0.46. CONCLUSION: The number of smoking-related prostate cancer deaths and DALYs continued to increase globally, whereas its ASMR and ASDR have been decreasing. This substantial progress is particularly significant in developed regions and vary across geographic regions. Medical strategies to prevent and reduce the burden should be adjusted and implemented based on country-specific disease prevalence.

[Effects of melatonin on oxidative stress and apoptosis-related gene signaling pathways following testicular torsion in rats].

OBJECTIVE: To investigate the effects of melatonin on the oxidative stress and signaling pathways of apoptosis-related genes following testicular torsion/detorsion in male rats. METHODS: Twenty-four healthy male Sprague-Dawley rats were randomly divided into a control, a torsion and a melatonin group of equal number. The torsion model was made in the animals of the latter two groups by 720° torsion of the left testis for 2 hours. The rats of the torsion and melatonin groups received intraperitoneal injection of isotonic saline and melatonin (17 mg/kg) respectively at 15 minutes prior to detorsion. At 24 hours after modeling, testis tissues were collected from the rats for detection of the apoptosis of the germ cells by flow cytometry (FCM), analysis of the expressions of Fas, Fas ligand (FasL) and Bax mRNA by quantitative real-time PCR (qRT-PCR), measurement of the cytochrome C content released from the mitochondrion by Western blot, and determination of the total antioxidant capacity (T-AOC) and the levels of myeloperoxidase (MPO) and malodialdehyde (MDA) by spectrophotometry. RESULTS: Compared with the torsion group, the rats treated with melatonin showed significantly increased normal testicular cells (ï¼»77.81 ± 6.52ï¼½% vs ï¼»88.61 ± 7.93ï¼½%, P < 0.05), decreased early apoptotic germ cells (ï¼»16.74 ± 3.16ï¼½% vs ï¼»6.97 ± 1.65ï¼½%, P < 0.05), down-regulated expressions of Fas (ï¼»4.52 ± 0.29ï¼½ vs ï¼»2.66 ± 0.37ï¼½, P < 0.01), FasL (ï¼»2.82 ± 0.30ï¼½ vs ï¼»1.73 ± 0.18ï¼½, P < 0.01) and Bax mRNA (ï¼»2.39 ± 0.18ï¼½ vs ï¼»1.50 ± 0.14ï¼½, P < 0.01), reduced levels of cytochrome C (ï¼»1.40 ± 0.38ï¼½ vs ï¼»0.67 ± 0.30ï¼½, P < 0.01), MPO (ï¼»0.52 ± 0.15ï¼½ vs ï¼»0.19 ± 0.10ï¼½ U/g prot, P < 0.01) and MDA ï¼»6.37 ± 1.73ï¼½ vs ï¼»3.98 ± 0.90ï¼½ nmol/mg prot, P < 0.01) and elevated T-AOC (ï¼»0.76 ± 0.25ï¼½ vs ï¼»1.55 ± 0.32ï¼½ U/mg prot, P < 0.01). CONCLUSIONS: Melatonin has a significant protective effect on spermatogenesis after testicular torsion by regulating the expressions of apoptosis-related genes and increasing T-AOC in the testis tissue.